Ecological Indicators 143 (2022) 109354 Available online 29 August 2022
1470-160X/© 2022 The Author(s). Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by- nc-nd/4.0/).
Temperature effects in single or combined with chemicals to the aquatic organisms: An overview of thermo-chemical stress
Syed Shabi Ul Hassan Kazmi , Yolina Yu Lin Wang , Yan-Er Cai , Zhen Wang *
Guangdong Provincial Key Laboratory of Marine Disaster Prediction and Prevention, and Guangdong Provincial Key Laboratory of Marine Biotechnology, Shantou
University, Shantou 515063, China A R T I C L E I N F O
Keywords:
Climate change Thermal stress Aquatic ecosystem Temperature dependent chemical toxicity
Aquatic organisms A B S T R A C T Climatic change (global warming) not only limited to the terrestrial environmental variations but also trans forming the aquatic environments. Recent studies have reported that both coastal and freshwater bodies have experienced the progressive warming and will intensify (giant leap) during this century. Same time the bewil dering array of thermal stresses poses serious threats to the aquatic organisms. Although, there is a growing body of literature and scientific consensus regarding the effects of temperature to the aquatic biota. Hitherto, the extent to which the thermo-chemical stress on aquatic organisms intensifying is not fully elaborated. We have summarized following declarations:
• Temperature variations induce a range of physiological and biological responses in aquatic organisms including; corticosteroid response, metabolic response, immune responses, heat shock proteins, and wavering in haemolymph parameters.
• The observed responses due to temperature fluctuations are actually attributed to the whole organism level performances like, acclimation and adaptation, fitness, feeding and food conversion ratio, growth and development.
• Temperature dependent chemical toxicities are subjected to influence the chemical processes and underlying molecular/genetic mechanisms of aquatic organisms at individual population and community levels.
Additionally, this review outlined the series of mechanisms in aquatic organisms associated with temperature changes in single or combined with chemicals. These observations provide significant evidence that the climate change and temperature variations are critical and there is pressing need to carefully evaluate the conditions and responses at large geographical scales.
1. Introduction In this century, climate change (global warming) may be the largest anthropogenic disturbance ever placed on natural systems (Sala et al.,
2000; Thomas et al., 2004). Climatic changes not only rising the water temperature also leads to more frequent and long-lasting cold and heat waves. As postulated, global warming will result in climate change which is more unpredictable with increasing extreme weather events, including larger temperature fluctuations and more frequent extreme temperature events occurring in the future (IPCC, 2014).
Climate change induced by temperature variations can profoundly influence the ecology of ectotherms, including their physiological, biochemical and ecological responses (Calosi et al., 2008). The rela tionship between ectotherm life-history performances and temperature is typically characterized by an unimodal thermal performance curve (TPC) (Huey and Stevenson, 1979), defining the optimum temperature (To) and the operative temperature range between the critical minimum temperature (CTmin) and the critical maximum temperature (CTmax).
Currently, this unimodal TPC has been commonly used to assess the sensitivity of ectotherm species to climate warming (Amarasekare and
Savage, 2012), composite fitness metrics such as reproduction, devel opment, metabolic rate, fitness (Van der Have, 2002; P¨ortner and Knust,
2007; Kingsolver, 2009), and evolution (Huey and Kingsolver, 1989;
Huey et al., 2003; Frazier et al., 2006).
* Corresponding author.
E-mail address: zhenwang@stu.edu.cn (Z. Wang).
Contents lists available at ScienceDirect Ecological Indicators journal homepage: www.elsevier.com/locate/ecolind https://doi.org/10.1016/j.ecolind.2022.109354
Received 21 July 2022; Received in revised form 15 August 2022; Accepted 18 August 2022
Ecological Indicators 143 (2022) 109354 2 Temperature variations caused by climate change, especially for thermal extremes, also have profound implications on chemical toxicity to individual organisms, and thus influences the size and structure of their population, the species composition of communities, and the structure and functioning of ecosystems (Cairns et al., 1975; Cairns et al., 1978; Lau et al., 2014; Zhou et al., 2014). Pioneer studies of the temperature-dependent chemical toxicity (TDCT) conducted on a wide range of aquatic organisms and chemicals have demonstrated that chemical toxicity and temperature varied from no relationship to negative or positive relationship which means that chemical toxicity partly, or fully dependent on temperature variations (Cairns et al., 1975;
Cairns et al., 1978). Although it is commonly reported that the chemical toxicity increases with increasing temperature (linear model, Model-I) within a range of temperatures (Leung et al., 2000; McConnachie and
Alexander, 2004; Kwok and Leung, 2005). As demonstrated in further comprehensive toxicity studies, non-linear function (e.g., inverted V- shape model, Model-II) tend to describe the relationship between tem perature and chemical toxicity more adequately, especially under extreme thermal conditions (Heugens et al., 2003; Bao et al., 2008).
Most recently, considering these two models (Model-I and Model-II) and natural temperature variations, the previous commonly used assessment factors (e.g. 10) were re-assessed to further validate whether or not the application of these factors in water quality guidelines (WQGs) can adequately protect freshwater and marine ecosystems, respectively (Lau et al., 2014; Zhou et al., 2014).
Because aquatic organisms are constantly exposed to environmental stimuli including both physical (temperature) and chemical stressors.
Temperature variations will not only alter the chemical toxicity to in dividual aquatic organisms, but also potentially introduce bias into the risk assessment of chemical contaminants or derivation of appropriate
WQGs for protecting the aquatic communities against chemicals. Thus, it is pertinent and essential to address the thermal effect on physico chemical properties of chemical contaminants and biological responses, and the combined influence of temperature and chemical exposure to biological responses. Therefore, this review emphasized the following three issues: 1) effects of temperature on physiological and biochemical responses to the aquatic organisms; 2) effects of tempeturure on chem ical preocess, including chemical speciation, accumulation, circulation and elimination; and 3) combined influence of temperature and chem ical to biological responses.
2. Temperature effects on aquatic organisms 2.1. Physiological and biological responses
2.1.1. Corticosteroid response Physiological stress responses such as cortisol release are simply autonomic responses that indicate activity and do not necessarily equate to suffering and diminished welfare (Ashley, 2007). The primary func tion of cortisol is to induce physiological changes that help animals either protect themselves from, or adapt to, the stressor. Cortisol release is a well-studied and sensitive indicator of cold stress. For instance, cortisol levels have been found to be positively correlated to the magnitude of temperature decreases for a number of fishes, including rainbow trout Oncorhynchus mykiss (Barton and Peter, 1982), salmon
Salmo salar (Skjervold et al., 2001; Hyv¨arinen et al., 2004), tilapia
Oreochromis aureus (Chen et al., 2002), and yellow perch Perca flavescens (Jentoft et al., 2002), and common carp Cyprinus carpio (Jaxion-Harm and Ladich, 2014). However, continuous high levels of cortisol can become maladaptive by regulating a diverse array of systems including metabolism, ion regulation, immune, growth and reproduction, which may ultimately affect the animal’s health (Houghton and Matthews,
1990). In certain instances, stress-modifying factors that are themselves chronically stressful, such as poor water quality or toxicants, can actu ally exacerbate (Barton and Peter, 1982) or attenuate the cortisol response to a second stressor. In rainbow trout (Salmo gairdneri), for instance, cortisol not only inhibits ovarian growth but also pushes the sex ratio in the male direction (van den Hurk and van Oordt, 1985).
2.1.2. Heat shock proteins (HSPs) One of the molecular responses that is activated in a cell under thermal stress is the heat shock proteins (HSPs) response, an event of genetic activation that occurs in the cells in response to abnormal, stressfully high or low temperatures (Hofmann, 2005). HSPs protect proteins, membranes, and other cellular components during heat-stress and facilitate repair or degradation of damaged proteins following a stressful event (Parsell and Lindquist, 1994). Importantly, while HSPs were so named because they are up-regulated by an acute increase in temperature (Lindquist, 1980). Extensive research has led to a detailed understanding of HSPs regulation and their mechanisms of action (Feder and Hofmann, 1999). There is a tendency of HSPs (e.g., HSP70) to in crease their expression with increasing levels of temperature variability (Arias et al., 2011; Folguera et al., 2011).At low temperatures, the synthesis and expression of HSP70 also occurs after the freezing point.
Because the depressed organism’s metabolism in such conditions can,t activate the physiological machinery which is necessary to start the synthesis of chaperone proteins, which occurs primarily in the recovery time. This indicating that there is a close relationship between the increased expression of HSP70 and the enhanced capacity of self- protection for subsequent extreme events (Krebs and Bettencourt,
1999; Chown and Nicholson, 2004).
2.1.3. Metabolic response Glucose concentration in the haemolymph increased during the exposure to the higher water temperatures (Lorenzon et al., 2007; Malev et al., 2010). This suggests that more glucose being made and available as energy supplement to meet increasing metabolic demand during stressful conditions of lower oxygen availability (Wendelaar Bonga,
1997) and is supported by the same temperature related response of lactate, which increases with increased energy usage with higher tem peratures (Durand et al., 2000; Ridgway et al., 2006; Lorenzon et al.,
2007). Results of haemolymph glucose in Maia squinado acclimated at different temperatures also indicated that the concentration of glucose in haemolymph reduced at low temperatures, while short acclimation periods at high temperature resulted higher glucose levels in the hae molymph (Durand et al., 2000).
2.1.4. Haemolymph parameters Hemocytes play an essential role in physiology and immune defense of aquatic organisms (Johansson et al., 2000). Loss and damage of circulating hemocytes would depress the immune ability, increase the susceptibility against pathogens, and even endanger the survival (Cheng et al., 2005). The total haemocyte count (THC) was found to be increased during exposure to the high temperatures so as to increase the immunity for thermal stress (Liu et al., 2010; Malev et al., 2010). Hae moglobin (Hb), as a direct link between ambient O2 availability and aerobic metabolism, also followed a temperature-dependent manner for aquatic invertebrates (Lamkemeyer et al., 2003; Seidl et al., 2005; Zeis et al., 2013). At temperatures below the critical thresholds, Hb induction in Daphnia is an example of a stressor-specific homeostasis response (Kültz, 2005). This second line of stress defense results in restored cellular oxygen conditions. However, such observations were not made by other authors for vertebrates (e.g., fishes), indicates that this attribute is not uniquely associated with heterothermy, but may have arisen in response to alternative evolutionary incentives (Clark et al., 2010;
Muyssen et al., 2010).
2.1.5. Immune responses The susceptibility of fish to disease is partly dependent on their environment, in particular on water temperature (Le Morvan et al.,
1998), because their entire physiology, including immune functions, is influenced by environmental temperature (Fry, 1967). For example,
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Ecological Indicators 143 (2022) 109354 3 most infectious diseases, such as the spring viraemia of carp (Cyprinus carpio), occur at lower environmental temperatures. Thus, the patho logical situation in fish depends both on temperature-dependent im mune system regulation and on pathogen growth (Le Morvan et al.,
1998). It is generally reported that lower temperatures adversely affected both cellular and humoral specific immune responses in various fish species (Bly and Clem, 1992). Lower temperatures can adversely affect specific immune responses mediated by T helper cells. In contrast, the secondary response can be elicited at low temperatures if immuno logical memory is established at high temperatures. The specific im mune responses, especially the humoural responses, are suppressed through the inhibition of the primary antibody responses at lower temperatures (Avtalion et al., 1970; Bly and Clem, 1992). In contrast, higher temperature could increase plasma IgM concentration, but a decreasing trend was observed in lysozyme activity and complement bacteriolytic activity in responses to thermal treatments (Jokinen et al.,
2011).
2.2. Whole-organism level performances 2.2.1. Acclimation and adaptations
Although physiological processes of aquatic ectotherms generally operate optimally within narrow temperature ranges, an extensive literature shows that most ectotherms can adjust or acclimate to changes in ambient temperature (Huey and Berrington, 1996; Stillman, 2003).
Within the genetic limits, sufficient acclimation of an organism can alleviate stress response to a novel thermal environment and thus extend thermal tolerant boundaries (Cairns et al., 1975; Cairns et al., 1978). As short-term exposure to either cold or warm extremes can be crucial to ectotherms (Bokhorst et al., 2008), they have to adjust their physio logical and biochemical responses so as to overcome such a stressful thermal scenario.
Stress proteins such as heat shock proteins (HSPs) can be induced to protect cellular structures (e.g., DNA) and to repair damaged compo nents, and in this way the ectotherm could extend its survivability even though in a time-limited manner (P¨ortner, 2002b). Liu et al. (2010) showed that anthraquinone extracts could improve haemolymph total protein contents, nitrogen monoxide concentrations, and lysozyme ac tivities, help shrimp resist high temperature stress. Additionally, Lub zens et al. (1995) found that the acclimation period of rotifers (Brachionus plicatilis) was associated with the synthesis of at least one specific protein (immunoisolation) and accumulation of lipids (eicosa pentaenoic acid), which supports the hypothesis of specific adaptations to survival at low temperatures during an acclimation period.
However, acclimation is generally considered to be only partial, so that physiological (and functional) processes are not completely de- coupled from temperature (Kingsolver and Huey, 1998). Fast and pro gressive temperature change could minimize acclimation phenomena (Burleson and Silva, 2011) and involved in a shift of thermal tolerant threshold (Frederich and P¨ortner, 2000). The common frog (Rana tem poraria) for instance did not show any behavioral adaptations in terms of breeding at lower temperatures (below 5 ◦C) (Muir et al., 2014).
2.2.2. Feeding and food conversion ratio (FCR) The influence of temperature-induced changes in water viscosity on the species activities (e.g., swimming) play an important role in deter mining the food uptake and feed conversion ratio (FCR) (Loiterton et al.,
2004), especially for small aquatic ectotherms. It is known that ambient temperature has mechanical effects on aquatic ectotherms by inversely affecting the dynamic viscosity of water (Vogel, 1994). For instance,
Bolton and Havenhand (1998) demonstrated that both physiological and viscosity-induced components of the reduction in water tempera ture could significantly reduce the number of microspheres ingested by
Galeolaria caespitosa. Likewise, Loiterton et al. (2004) demonstrated that the ingestion rate of D. galeata was found to be 50 % lower at 10 ◦C than at 25 ◦C due to the combined effects of increased viscosity and lower temperature, while viscosity alone accounted for 61 % of the decline in
FCR. Lagergren et al. (2000) also showed that hydrodynamic costs of predator defense in Eubosmina increased at low temperatures due to increased drag associated with higher viscosities.
Evidence also showed that growth of aquatic individuals were opti mized at the optimum temperature, in combination with maximum food intake and optimum FCR (Abbink et al., 2012; Vellinger et al., 2012). A reduction in feed utilization efficiency at extreme water temperatures has been reported for barramundi Lates calcarifer (Bermudes et al.,
2010), wolf fish Anarhichas lupus (Imsland et al., 2006) and European seabass Dicentrarchus labrax (Person-Le Ruyet et al., 2004). This is also consistent with another study on yellowtail kingfish in which FCR was significantly better in warm water (17 ◦C to 22 ◦C) compared with cool water (14 ◦C to 17 ◦C) (Moran et al., 2009). This can be explained that activities of digestive enzymes increase with within a certain tempera ture range but shortened passage time at higher temperatures may reduce exposure of food to enzymatic action (Harwood, 1979; McCarthy et al., 1999).
2.2.3. Reproduction Reproductive traits (e.g., eggs, hatching) are thought to be more sensitive to thermal stress than other traits and should therefore be included when estimating the fitness effects of thermal stress (Jørgensen et al., 2006). Moreover, reproductive processes are often affected by temperature change earlier, in other words by less severe conditions than those affecting development and survival (Fasolo and Krebs, 2004).
Previous studies also show a more symmetric temperature response on reproductive performances predicted by reaction rate theory (i.e., enzyme kinetics) (Carriere and Boivin, 1997; Dannon et al., 2010;
Amarasekare and Savage, 2012), in combination with the regulatory processes based on negative feedback pathways such as hormonal regulation (Nijhout, 1994). Several studies have investigated the nega tive effects of heat shock on the longevity and fecundity heat or cold shock processes (Rinehart et al., 2000). Heat or cold shock can also cause injury to oocytes and ovarian development in females that lead to the decrease in egg production (Rinehart et al., 2000; Castro-Longoria,
2003). In addition, heat shock can cut down on male fertility due to direct injury to the testes and sperm (Scott et al., 1997; Nguyen et al.,
2013). Moreover, the hatching success is also adversely influenced by extreme higher or lower temperatures (Holste and Peck, 2006; Hansen et al., 2010; Cruz et al., 2013), leading to lower survivor and hence lowering abundances of aquatic organisms. This probably due to decreased membrane permeability, disequilibria of coupled enzyme reactions and limits imposed by kinetics and inactivation of enzyme proteins (Rosa et al., 2012).
2.2.4. Growth and development Water temperature is one of the major environmental factors influ encing growth and development in aquatic ectotherms (Brett, 1979). A decreasing ontogenetic shift in optimum temperature is common for most ectotherms and has been described for a range of marine fishes including Atlantic cod (G. morhua) (Lafrance et al., 2005); turbot (Scophthalmus maximus) (Imsland et al., 1996); Atlantic halibut (Hippo glossus hippoglossus) (Hallaråker et al., 1995); plaice (Pleuronectes pla tessa) (Fonds et al., 1992); and yellowtail (Seriola lalandi) (Pirozzi and
Booth, 2009; Abbink et al., 2012). The growth of fishes were then reduced at the extreme temperature compared with the optimal tem perature (i.e., Inverted V-shape Model-II). This parabolic temperature response is typical of all species and can be explained by that the sig nificant reduction in food intake coupled with an increased demand for energy at such high temperatures is the likely major factor contributing to the poor growth performance of the fishes at extreme high tempera tures (Imsland et al., 1996; Peck et al., 2002; Bermudes et al., 2010). On the contraty, loss of appetite was suggested to be the direct reason for the growth inhibition at low temperatures (Ibarz et al., 2005). In addi tion, the fishes would have restricted heart rate and circulation of blood,
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Ecological Indicators 143 (2022) 109354 4 leading to limited supply of oxygen and energy to maintain essential cellular functions, and such conditions force the fish to switch to anaerobic respiration to acquire more energy (P¨ortner, 2002a), and hence, lower growth performances at extreme low temperatures.
Previous studies also showed that speices’ developmental rates exhibited temperature responses that were most consistent with the left- skewed inverted V-shape pattern (Sharpe and DeMichele, 1977; Huey and Berrigan, 2001; Gillooly et al., 2002; Savage et al., 2004). Typically, development ceases below a lower thermal threshold. Above it, the rate of development increases with temperature until an optimum is reached.
Above the optimal temperature, the rate rapidly decreases to zero (Campbell et al., 1974; Briere et al., 1999; Van der Have, 2002). This pattern has been attributed to the reaction rate and high temperature inactivation of a single major enzyme that drives the developmental process (Van der Have and de Jong, 1996; Van der Have, 2002; Rat kowsky et al., 2005); that is, the reaction rate increases monotonically with temperature while enzyme inactivation exhibits a unimodal response to temperature.
2.2.5. Survivorship and mortality The survivorship of free-living stages of auqatic organisms are likely to be affected by temperature effects on resource acquisition (Van der
Have, 2002). Thermal stress can become lethal to an aquatic organism when the temperature exceeds its thermal tolerance limit, which is determined by the interplay of its life stage, physiological condition, genetic history, and environmental influences (Cairns et al., 1975). The cumulative survivorship, especially embryonic viability, exhibits a temperature response that is inverted U-shaped rather than left skewed (Van der Have, 2002; Angilletta, 2009; Kingsolver, 2009), and per capita mortality rates exhibit a monotonic temperature response (Gillooly et al., 2001; Savage et al., 2004), this is supported by some studies that mortality rates can increase at very low or high temperatures (Morgan et al., 2001; Kyprianou et al., 2010; Wexler et al., 2011; Li et al., 2014a).
Extreme temperature-induced mortality can be explained by the oxygen limiting theory that fish have restricted ventilation rate at cold, resulting in a decline of oxygen supply to various organs, while the temperature- driven mismatch in energy demand and supply, and decrease of oxygen solubility in warm waters concomitantly challenge the survivability of the fish at extremely warm conditions (P¨ortner and Knust, 2007).
2.2.6. Fitness In ectotherms, fitness is also strongly temperature dependent: increasing temperature causes a rise in fitness up to a maximum, fol lowed by a rapid decline in fitness as temperature increases further (Kingsolver, 2009). This dependence provides a quantifiable metric for assessing the effects of climate warming on population viability. Since fitness is a composite trait consisting of individual components (e.g., fecundity, development, survivorship), Amarasekare and Savage (2012) also developed a mathematical framework that partitions the tempera ture dependence of fitness into its components of fecundity, develop ment, and mortality. Because the qualitative properties of the temperature responses of fitness components are robust to taxonomic and geographic variation (Gillooly et al., 2001; Gillooly et al., 2002;
Savage et al., 2004). The “hotter-is-better” hypothesis suggests a specific type of concerted change. Hotter-is-better proposes that genotypes or species with relatively high optimal temperatures (To) also have rela tively high maximal performance or fitness (rmax) at the optimum (Hamilton, 1973; Angilletta et al., 2010). This is based on the thermo dynamic argument that reaction rates of active enzymes increase with absolute temperatures, such that maximum reaction rates for species adapted to hot temperatures will be higher than those for species adapted to cold temperatures (measured at the optimal temperature for each) (Frazier et al., 2006; Kingsolver and Huey, 2008). As a result, the increase in fitness up to that optimum temperature is much slower than the decrease in fitness when environmental temperatures exceed the optimum (Deutsch et al., 2008), and the maximum potential fitnesses of adapted organisms will be greater in a warmer than in a cooler world (Kingsolver, 2009).
Temperature affects biochemical rates by altering the kinetic and free energies of biochemical reactions. For enzyme- mediated reactions, there are two components to the temperature dependence of reaction rates. First, increasing temperature increases the catalytic rate for an enzyme in its active state by increasing the kinetic energy of the system, as described by the Eyring (1935) model. The quantitative effect of temperature predicted by the Eyring model is best described using an
Arrhenius plot, relating the inverse of (absolute) temperature (T) to the reaction rate (Arrhenius 1889). The second component is the probability that the enzyme is in its active state. In general, this probability is maximal at some intermediate temperature and declines at higher and lower temperatures as a result of both reversible and irreversible enzyme inactivation (Ratkowsky et al., 2005). These two factors combine to give the thermal sensitivity of reaction rates a characteristic shape. At low temperatures, reaction rates increase linearly to geometrically with increasing temperature, reach a maximum at some “optimal” tempera ture, and then decrease rapidly at temperatures above the optimum. As a result, thermal sensitivity of reaction rates is strongly asymmetric at temperatures below versus above the optimum.
Remarkably, most biological rate processes at the whole-organism level, including rates of locomotion, growth, development, and fitness, exhibit the same basic form of thermal sensitivity as biochemical reac tion rates (Huey and Stevenson, 1979; Angilletta, 2009). As a result, models for the thermal sensitivity of biochemical reaction rates can be readily adapted to model the thermal sensitivity of organismal perfor mance and fitness (Ratkowsky et al., 2005). This common overall shape provides a useful means of identifying important patterns, or “modes,” of variation in thermal performance curves (TPCs) for organismal per formance or fitness among genotypes, populations, or species (Huey and
Kingsolver, 1989).
3. Temperature-dependent chemical toxicities (TDCT)
Climate change induced temperature variations, especially for ther mal extremes can have a profound implications on chemical toxicity to ectothermic organisms. Temperature-dependent chemical toxicity (TDCT) studies on wide ranges of aquatic organisms and chemicals have demonstrated that chemical toxicity and temperature varied from no relationship to negative or positive relationship (Cairns et al., 1975;
Cairns et al., 1978). Despite it is commonly reported that chemical toxicity increases with increasing temperature (i.e., Linear Model-I) (Leung et al., 2000; McConnachie and Alexander, 2004; Kwok and
Leung, 2005), non-linear function can describe the relationship between temperature and chemical toxicity more adequately with a wider range of temperatures (Angilletta, 2006; Bulte and Blouin-Demers, 2006; Bao et al., 2008). For example, chemical toxicity is found to follow a cumulated U-shape relationship and lowest at an optimal temperature (Topt) (Bao et al., 2008; Sangita et al., 2012). The inverse V-shape relationship (i.e., Model-II) between temperature and chemical toxic ities was also commonly observed in freshwater species (Lau et al.,
2014) and marine species (Zhou et al., 2014). Following the Model-II, chemical toxicity to aquatic organisms at a low temperature generally decreased with increasing temperature until it reached the optimal temperature, from which onwards it started to increase with rising temperature. In general, aquatic organisms living in optimal conditions are more tolerable to chemical toxicity than those living in the condi tions near to their thermal tolerance limits (Heugens et al., 2001; Bao et al., 2008; Li et al., 2014a).
3.1. Temperature-mediated chemical processes Chemical toxicity to aquatic organisms is not only associated with the concentration of the chemical in the water but also closely linked to its speciation and bioavailability (Bourgeault et al., 2013). Temperature
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Ecological Indicators 143 (2022) 109354 5 can also influence partition coefficient or diffusion rates chemicals (Heugens et al., 2001), leading to aggregation and precipitation, and then influences their speciation, solubility and bioavailability (Bour geault et al., 2013), resulting in significant alterations in their joint toxicities to an aquatic organism (Brocchi et al., 2013). The generally observed temperature-toxicity relationship was also partly thought to be related to changes in accumulation kinetics (Heugens et al., 2003).
Because the bioavailability of chemicals to aquatic species is controlled by chemical thermodynamics (i.e., chemical speciation) in the water, and then influenced by bonding interaction kinetics between ions or their complex species of the ions with the cell wall (Benda and Kouba,
1991).
It is generally accepted that a higher temperature increases the rate of uptake of chemical contaminants via increases of metabolic rate and ventilation rate of ectotherms and hence boosts bioaccumulation of the chemicals in the body tissue (Tsui and Wang, 2006; Cherkasov et al.,
2007; Schiedek et al., 2007), and ultimately leading to higher chemical toxicity at the higher temperature levels. Taken cadmium for an example, higher cadmium body concentrations at elevated temperature were reported for several species, such as Hexagenia rigida (Andres et al.,
1998), Asellus aquaticus (Vann Hattum et al., 1993), Corbicula fluminea (Graney et al., 1984), Anguilla japonica (Yang and Chen, 1996), Daphnia magna (Stuhlbacherl et al., 1993; Heugens et al., 2003), Perca fluviatilis (Edgren and Notter, 1980) and Chironomus riparius (Bervoets et al.,
1993). On the contraty, those fishes grown at lower temperatures had significantly lower osmolality than those grown at the optimum tem perature, which was due primarily to a significant reduction in plasma
Cl-, in combination of lower Na+/K+-ATPase activity at the extreme low temperatures. This is the expected response to the increased drinking and ion uptake rates associated with the increase in metabolism seen with increasing temperature (Ando et al., 2003). Moreover, the high test chemical concentrations could also inhibited the normal functioning of the the test speceis at the higher temperature levels, hampering a further increase in the cadmium uptake rate (Heugens et al., 2003).
Temperature may also affect physiological and biochemical state of an organism and thereby influence the partition of chemicals over the different compartments of the organism. Biochemical detoxification and elimination can also be increased with temperature, leading to a reduction of chemical toxicity. Additionally, ectotherms could enter dormancy (i.e., metabolic depression) at low temperatures leading to a reduced uptake of chemical and hence lowering toxicity (Bao et al.,
2008). In contrast to uptake rates, the temperature dependence of chemical (e.g., cadmium) elimination appears to be more complex. For instance, the depuration rates of Asiatic clams on cadmium were not altered by temperature (Inza et al., 1998). However, Burrowing mayfly nymphs eliminated cadmium rapidly when temperature was elevated (Odin et al., 1997), while a small but significant temperature effect on cadmium elimination was also reported in freshwater isopods since the metal was eliminated at 5 ◦C but not at 10 and 20 ◦C (Vann Hattum et al.,
1993). Generally, the temperature-toxicity relationship for chemicals demonstrates that elevated temperatures tend to enhance toxic effects of chemicals on organisms, which may be (partially) explained by the higher uptake rate of metals and a higher intrinsic sensitivity of organisms.
3.2. Temperature-mediated mechanisms Most freshwater creatures are ectothermic and their metabolism is highly temperature-dependent (Cherkasov et al., 2006), also making temperature a key environmental factor in controlling their physiolog ical performances, such as species inhabiting and acclimation (Burleson and Silva, 2011), resource acquisition (Van der Have, 2002), ventilation (Vellinger et al., 2012) and thus fitness (e.g., settlement, development, survivorship, reproduction) (Frazier et al., 2006; Angilletta, 2009;
Kingsolver, 2009; Amarasekare and Savage, 2012). Temperature can also affect various physical parameters in water bodies under different thermal dynamics. For example, the decreasing of gas solubility (e.g., oxygen) in aquatic organisms under the extreme high or low tempera tures would induce physiological and biological damages to aquatic ectotherms (P¨ortner, 2002a). Moreover, the lower temperature-induced changes in water viscosity can influence the swimming performance and kinematics of ectotherms (Fuiman and Batty, 1997), and then decline food ingestion (Bolton and Havenhand, 1998; Loiterton et al., 2004) and food conversion ratio (Liu et al., 2010; Abbink et al., 2012). Every aquatic organism has a thermal tolerance range (TTR), which is deter mined by interplay of developmental, genetic and environmental factors (Cairns et al., 1975). When temperature is higher or lower than the TTR of an organism, lethality may occur, and such a thermal stress at tem perature extremes may further increase the toxicity of a chemical.
Therefore, such an integrative inverted V-shape response (include
Model-I) can be typically explained by the temperature-regulated mechanisms.
Oxygen has long been known to play an important role in setting acute temperature limits of animals but characterizing the temperature limits of the physiological and biochemical pathways associated with the oxygen supply cascade. Oxygen-limited thermal tolerance (OLTT) model describes more details in physiological activities of ectotherms when exposed to various temperatures (Frederich and P¨ortner, 2000;
P¨ortner, 2001). The OLTT model suggests that aquatic ectotherms, like fishes, generally live within a confined range of temperatures where they function aerobically without displaying any sign of stress (e.g., behavioral disorder), beyond the confined range, however, the ecto therms would encounter a mismatch of energy demand and supply, and eventually shift to anaerobic respiration at the extreme high or low temperatures so as to increase energy supply for sustaining essential cellular and physiological functions (P¨ortner, 2010). Furthermore, thermal changes co-occurred progressive carbon dioxide accumulation would also exaggerate hypoxia due to the elevated oxygen demand on the one hand, and lower oxygen solubility at high temperatures on the other (Brewer and Peltzer, 2009; P¨ortner, 2010). When such changes in temperature and oxygen concentration are introduced, total meta bolism, basal metabolism and scope of activity of aquatic organisms decrease, while the frequency of locomotory acts and mechanical power decline (Svetlichny et al., 2000). Evidence showed that oxygen defi ciency could elicit (1) the transition to passive tolerance and associated systemic and cellular stress signals such as hormonal responses or oxidative stress; and (2) the activation of protection mechanisms (e.g., heat hock proteins) at thermal extremes (P¨ortner and Knust, 2007;
P¨ortner, 2010). Because reduction in oxygen consumption rates may be directly linked to chemical induced mucus production, structural dam age to gills and reduction in oxygen carrying capacity of haemocyanin (Leung et al., 2000; Morley et al., 2012). Therefore, it is easy to un derstand oxygen deficiency in the body tissue results in changes in growth, survival, reproduction and even population distribution and abundance under thermal stress (Perry et al., 2005; P¨ortner, 2010).
The increased bioaccumulation of chemical compounds is also bound to cause physiological discomfort or damage to organisms, and thus temperature can influence their susceptibility to chemical exposure (Cairns et al., 1975; Heugens et al., 2001). Reactive oxygen species (ROS) are normal byproducts of cellular respiration and have important roles in cell signalling and homeostasis (Cadenas, 1989). Nonetherless, during times of thermal stress, the oxygen mismatch may thus be due to physiological hypoxia (Cadenas, 1989; Matschak et al., 1995), which subsequently induces ROS and oxidative stress (Lesser, 2006; Vinagre et al., 2012; Vinagre et al., 2014). It has been well-documented that thermal stress is positively correlated with oxidative stress in aquatic ectotherms species (Dahlhoff et al., 1991; Paital and Chainy, 2014). This is further supported by the response of the oxidative stress biomarkers (e.g., SOD, CAT, GPX) which were commonly reported to be the lowest at the optimal temperature and it increased outside the speices upper and lower optimum thermal limits (Vinagre et al., 2012; Vinagre et al.,
2014), suggesting organisms suffer higher influences from high or low
S.S.U.H. Kazmi et al.
Ecological Indicators 143 (2022) 109354 6 temperatures than that from the optimum temperature. Thermal induced oxidative stress can also modify concentrations of lipid, protein and carbohydrate, leading to the changes of partition coefficients over membrane, storage lipid and body fluid (Heugens et al., 2001). Oxida tive stress is also known to be an important induction factor for cell apoptosis (Green and Reed, 1998; Orrenius, 2007). Previous researches demonstrated that water temperature decrease can induce ROS pro duction and hemocyte apoptosis (Qiu et al., 2001; Li et al., 2014b), in crease caspase-3 transcription and activity levels (Chang et al., 2009), cause DNA damage and lipid peroxidation (Malev et al., 2010; Vinagre et al., 2012), reduce the immune functions and resistance against pathogen infection (Le Morvan et al., 1998; Cheng et al., 2005; Chang et al., 2009). It is generally accepted that low temperatures adversely affect specific immune responses, especially the humoural response (Avtalion et al., 1970; Bly and Clem, 1992). Thus, the pathological sit uation in fish depends both on temperature dependent immune system regulation and on pathogen growth (Le Morvan et al., 1998).
4. Temperature dependent species sensitivity distribution (SSD)
Over the last twenty years, the chemical state of many water bodies have been improved due to the effective and precise risk mitigating strategies and measures. However, thermal stress and elevated tem perature have significant impacts on the aquatic environments. The elevated temperature most probably cause mortality of algal blooms or other aquatic species depends on the receiving water body (de Vries et al., 2008). Very earlier Carter et al. (1979) provided a rationale for evaluation of the biological responses induced by thermal stress. How ever, most of the times thermal stress coincide with various environ mental factors like antifouling agents, toxic biocides and hypoxia. Under these circumstances, it is problematic to evaluate the individual risk factor, thus integrating risk or multistress approach in overall one in dicator would be the more clear (De Zwart and Posthuma, 2005).
Therefore, the application of species sensitivity distribution (SSD) in combination with toxic and non-toxic stressors is more ideal indicator for ecological risk assessment.
Species sensitivity distribution describes the “mean sensitivity and range of sensitivity among biota” for specific type of the stressor (Aldenberg et al., 2002). This method is useful for the generic risk assessment, but also beneficial for location specific assessment if the local species incorporated (de Vries et al., 2008). Previously, the SSD was used by de Vries et al. (2008) to calculate the temperature induced mortality in aquatic environment as potential risk assessment tool of thermal stress. Their study summarized the acute exposure of organisms (50 aquatic species) that were capable of drift or swim in heated water.
Furthermore, the study revealed loss of the resident species that couldn’t sustain the warm temperature. Later on Zhou et al. (2014) focused on marine ecosystem and give a viewpoint to predict the temperature dependent chemical toxicity to marine organisms. Their study investi gated the temperature-acute toxicity correlation for variety of chemicals (e.g., chromium, cadmium, zinc, copper, nickel and TBT), on numerous marine ectotherms under various temperatures by two models (TDCT model I and II). However, the application of temperature dependent
SSDs on both models (TDCT model I and II), revealed that the marine water species were relatively more sensitive to the chemicals at high or low temperatures as compared to the optimal temperatures (Zhou et al.,
2014).
In the study of Mu et al. (2018) temperature and salinity based SSD was employed to predict the chemical toxicity of (i.e., Zn, Ni, Cd, Cu, Cr and Hg) on numerous communities of marine organisms. The sigmoidal logistic model on temperature-salinity based SSDs (represented by S type surfaces) demonstrated that the chemicals (metals) have high toxic potentials to the marine organisms. Furthermore, the physicochemical properties of the metals significantly affected their toxicities to the marine organisms. Both temperature and salinity actually affect the metals (chemicals) toxicities to the marine organisms and determine the slopes/shapes of SSD curves. In short, salinity affects the gradients of fitted curves while temperature influenced on horizontal positions (Mu et al., 2018). In an updated study on the application of temperature- dependent SSDs by Wang et al. (2019) reported that the thermal ex tremes can intensify the toxicity of chemicals (e.g., chlorpyrifos, carbaryl, mercury, copper, malathion, pentachlorophenol, and phenol) to freshwater biological communities. The temperature dependent SSDs generally showed the inverted V-shape (same as Model II) relationship along the temperature gradients. The application of temperature dependent SSDs however could be pivotal in refining the WQGs at various natural temperature ranges (Wang et al., 2019). Overall, SSD ascertain the logical standard to investigate the influence of numerous stressors or abiotic factors (e.g., temperature, salinity, pH etc.) on chemical toxicity to the aquatic organisms. However, rigorous studies combining the other stressors in one (aggregation of all stressors) would be more ideal choice to evaluate the chemical toxicity to aquatic biota and ecological risk assessment in both marine and freshwater environments.
5. Conclusion Thermal/temperature stress on aquatic organisms induce negative changes in their physiological and biochemical processes. The organ ism’s response to thermal extremes varies among different aquatic or ganisms at metabolic, hormonal and immunological levels. Higher temperature, disrupts the molecular and genetic mechanisms of organ isms, which leading toward abnormal individual performances. The negative biochemical responses (e.g., accumulation and release) signif icantly affect the organism’s adaptation, fitness, growth and develop ment, survivorship and reproduction activities. Furthermore, the thermal extremes can have profound implications on chemical toxicity to the aquatic organisms. Higher temperatures increases the rate of chemical contaminants uptake through increased metabolic and venti lation rate which subsequently boost the bioaccumulation of chemicals in the body tissues, ultimately leading to higher chemical toxicity.
Moreover, not the individual organisms are sensitive to the thermal stress, population, communities and whole ecosystem responds to the temperature extremes. This review, not only shed lights on temperature effects and temperature dependent chemical toxicity, it also provides a systematic approach to understand the drastic climate change scenario and combined thermo-chemical stress on aquatic ecosystems. However, extended and rigorous studies on domestic, regional and global levels are required to highlight the impacts of thermal stress, and devised advanced strategies to overcome this issue for sustainable aquatic environment.
CRediT authorship contribution statement Syed Shabi Ul Hassan Kazmi: Investigation, Methodology, Writing
– original draft. Yolina Yu Lin Wang: Writing – review & editing. Yan- Er Cai: Writing – review & editingZhen Wang: Conceptualization, Su pervision, Funding acquisition, Writing – review & editing.
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Data availability Data will be made available on request.
S.S.U.H. Kazmi et al.
Ecological Indicators 143 (2022) 109354 7 Acknowledgements
This work research was supported by the National Natural Science
Foundation of China, China (42177264), 2020 Li Ka Shing Foundation
Cross-Disciplinary Research Grant, China (2020LKSFG03E), and Shan tou University Scientific Research Foundation for Talents, China (NTF19044).
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