Heat shock induces oxidative stress in rotan Perccottus glenii tissues

The effects of temperature transition from 19 to 32 °C on oxidative stress indices and activities of the main antioxidant enzymes were investigated in the rotan, Perccottus glenii. Levels of lipid peroxides (LOOH), thiobarbituric acid-reactive substances (TBARS), low- (L-SH) and high-molecular mass (H-SH) thiols and activities of superoxide dismutase (SOD) and catalase were measured in rotan brain, liver and muscle over 1–12 h of high-temperature exposure followed by 3 or 24 h lower (19 °C) temperature recovery. Heat shock exposure during 1 h transiently increased 1.5–3.2-fold LOOH levels in rotan tissues with subsequent suppression of their content; however, 12 h exposure again increased LOOH levels in the brain. TBARS content were elevated by 2–3-fold during the entire heat shock exposure in the brain and liver. Levels of both products of lipid peroxidation were generally near control values during return to 19 °C. L-SH content was lowered during heat shock exposure in the brain, transiently increased after 6 h in the liver and almost disappeared after longer treatment in the muscle. Liver H-SH content slightly decreased under heat shock exposure, but was elevated after 6 h in the brain and muscle. In the latter case, L-SH level was below control values during recovery. SOD activities increased 2-fold in the liver after 6–12 h heat shock. Liver catalase activities decreased at the same conditions. Generally, a quick response to suppression of lipid peroxidation and possible involvement of its products in the up-regulation of antioxidant enzymes seem to be key adaptations to high temperature.     

Temperature increase results in oxidative stress in goldfish tissues. 2. Antioxidant and associated enzymes

Activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione-S-transferase (GST), glutathione reductase (GR), and glucose-6-phophate dehydrogenase (G6PDH) were measured in four tissues of goldfish, Carassius auratus L., over 1-12 h of high temperature (35 degrees C) exposure followed by 4 or 24 h of lower temperature (21 degrees C) recovery. SOD activity was strongly affected by heat shock, increasing 4-fold in brain, liver, and kidney, but was mainly reversed at recovery. In some tissues, activities of SOD, catalase, GPx, and G6PDH decreased significantly after 1 h heat shock exposure suggesting that thermal inactivation possibly occurred, but were renewed at further exposure. In many cases, 4 h of return to the initial temperature decreased enzyme activities. High correlation coefficients between SOD activities and levels of lipid peroxidation products suggest that these products might be involved in up-regulation of antioxidant defense. Several enzymes (SOD, GST, GR) responded to stress in coordinated manner.     

Hypoxia and recovery perturb free radical processes and antioxidant potential in common carp (Cyprinus carpio) tissues

The effects of hypoxia exposure and subsequent normoxic recovery on the levels of lipid peroxides (LOOH), thiobarbituric acid reactive substances (TBARS), carbonylproteins, total glutathione levels, and the activities of six antioxidant enzymes were measured in brain, liver, kidney and skeletal muscle of the common carp Cyprinus carpio. Hypoxia exposure (25% of normal oxygen level) for 5h generally decreased the levels of oxidative damage products, but in liver TBARS content were elevated. Hypoxia stimulated increases in the activities of catalase (by 1.7-fold) and glutathione peroxidase (GPx) (by 1.3-fold) in brain supporting the idea that anticipatory preparation takes place in order to deal with the oxidative stress that will occur during reoxygenation. In liver, only GPx activity was reduced under hypoxia and reoxygenation while other enzymes were unaffected. Kidney showed decreased activity of GPx under aerobic recovery but superoxide dismutase (SOD) and catalase responded with sharp increases in activities. Skeletal muscle showed minor changes with a reduction in GPx activity under hypoxia exposure and an increase in SOD activity under recovery. Responses by antioxidant defenses in carp organs appear to include preparatory increases during hypoxia by some antioxidant enzymes in brain but a more direct response to oxidative insult during recovery appears to trigger enzyme responses in kidney and skeletal muscle.     

Hypoxia induces oxidative stress in tissues of a goby, the rotan Perccottus glenii

The effects of hypoxia (0.4 mg O₂/L) for 2, 6 or 10 h and subsequent normoxic recovery on the levels of lipid peroxides, thiobarbituric acid reactive substances, protein carbonyls (CP), free thiols, and the activities of six antioxidant and associated enzymes were measured in the brain, liver, and skeletal muscle of the rotan Perccottus glenii. Hypoxia increased CP content in the brain (5.0–7.4-fold), liver (2.2–3.3-fold) and muscle (3.2–61-fold) relative to controls and the levels remained elevated during recovery. Lipid peroxide content rose within 2 h of hypoxia in all tissues examined with the most marked increase (8.7-fold) in the liver, but decreased again during longer hypoxic exposure except in the muscle. Levels of low-molecular mass thiols were transiently lowered after 2 h hypoxia in all tissues, but were higher compared with controls after longer hypoxic exposure and recovery. Hypoxia decreased protein thiol content in the liver and muscle that return to control levels during recovery. Experimental conditions affected enzyme activities in a different manner. Superoxide dismutase activity rose two-fold in the liver of hypoxic fish, and a similar tendency was seen in muscle glutathione-S-transferase. Activities of other enzymes were decreased or unchanged during hypoxia and elevated in some cases during normoxic recovery. Taken together, these data show that hypoxia resulted in the development of oxidative stress and a compensatory changes of antioxidant enzymes in the tissues.     

Oxidative stress and antioxidant defense responses by goldfish tissues to acute change of temperature from 3 to 23 °C

The effects of a rapid transfer from a low (3 °C) to a warm (23 °C) temperature on oxidative stress markers and antioxidant defenses were studied in the brain, liver and kidney of the goldfish, Carassius auratus. Cold-acclimated fish were acutely moved to 23 °C and sampled after 1, 6, 12, 24, 48 or 120 h of warm temperature exposure. Lipid peroxide levels increased quickly during the first few hours at 23 °C, but thiobarbituric acid-reactive substances changed little. Protein carbonyl content was reduced by 20–40% in the liver over the entire experimental course, but increased transiently in the kidney. The content of high-molecular mass thiols decreased by two-thirds in the brain and was affected slightly in other organs. By contrast, total low-molecular mass thiols (e.g. glutathione and others) increased transiently. Activities of the primary antioxidant enzymes—superoxide dismutase and catalase—were generally unaffected in goldfish organs, whereas glutathione-dependent enzymes were elevated in the brain and kidney after 24–48 h at 23 °C. Glutathione peroxidase increased by 1.5–2.3-fold and glutathione-S-transferase by 1.7-fold. Hence, a short-term exposure to warm temperature disturbed several oxidative stress markers, but only slightly affected the activities of antioxidant enzymes. However, comparison of the current data for cold-acclimated winter fish with the same parameters in summer fish suggests that longer exposure to high ambient temperature requires the enhancement of activities of glutathione-dependent enzymes for maintaining the steady-state levels lipid peroxidation and protein oxidation in goldfish tissues.     

Hyperoxia results in transient oxidative stress and an adaptive response by antioxidant enzymes in goldfish tissues

The effects of hyperoxia on the status of antioxidant defenses and markers of oxidative damage were evaluated in goldfish tissues. The levels of lipid peroxides, thiobarbituric acid reactive substances, carbonyl proteins and the activities of some antioxidant enzymes were measured in brain, liver, kidney and skeletal muscle of goldfish, Carassius auratus L., over a time course of 3-12 h of hyperoxia exposure followed by 12 or 36 h of normoxic recovery. Exposure to high oxygen resulted in an accumulation of protein carbonyls in tissues throughout hyperoxia and recovery whereas lipid peroxides and thiobarbituric acid reactive substances accumulated transiently under short-term hyperoxia stress (3-6 h) but were then strongly reduced. This suggests that hyperoxia stimulated an enhancement of defenses against lipid peroxidation or mechanisms for enhancing the catabolism of peroxidation products. The activities of principal antioxidant enzymes, superoxide dismutase and catalase, were not altered under hyperoxia but catalase increased during normoxic recovery; activities may rise in anticipation of further hyperoxic excursions. In most tissues, the activities of glutathione-utilizing enzymes (glutathione peroxidase, glutathione-S-transferase, glutathione reductase) as well as glucose-6-phosphate dehydrogenase, were not affected under hyperoxia but increased sharply during normoxic recovery. Correlations between some enzyme activities and oxidative stress markers were found, for example, an inverse correlation was seen between levels of thiobarbituric acid reactive substances and glutathione-S-transferase activity in liver and catalase and glucose-6-phosphate dehydrogenase in kidney. The results suggest that liver glutathione-S-transferase plays an important role in detoxifying end products of lipid peroxidation accumulated under hyperoxia stress.     

Oxidative stress and antioxidant defenses in goldfish Carassius auratus during anoxia and reoxygenation

The purpose of this work was to evaluate the response of the antioxidant system of goldfish Carassius auratus during anoxia and reoxygenation. The exposure of goldfish to 8 h of anoxia induced a 14% decrease in total glutathione levels in the kidney, although the liver, brain, and muscle were unaffected. Anoxia also resulted in increases in the activities of liver catalase, brain glucose-6-phosphate dehydrogenase, and brain glutathione peroxidase (by 38, 26, and 79%, respectively) and a decrease in kidney catalase activity (by 17.5%). After 14 h of reoxygenation, liver catalase and brain glutathione peroxidase activities remained higher than controls and several other tissue-specific changes occurred in enzyme activities. Superoxide dismutase activity was unaffected by anoxia and reoxygenation. The levels of conjugated dienes, as indicators of lipid peroxidation, increased by 114% in liver after 1 h of reoxygenation and by 75% in brain after 14 h of reoxygenation. Lipid peroxidation was unaffected in kidney and depressed during anoxia and reoxygenation (by 44-61%) in muscle. Regulation of the goldfish antioxidant system during anoxia may constitute a biochemical mechanism that minimizes oxidative stress following reoxygenation.     

Diethyldithiocarbamate injection induces transient oxidative stress in goldfish tissues

The effects of intraperitoneal injection of diethyldithiocarbamate (DDC) on free radical processes were examined in brain, liver and kidney of goldfish (Carassius auratus). Levels of oxidatively modified lipids and proteins as well as the activities of antioxidant and associated enzymes were measured. Intraperitoneal injection of DDC at a concentration of 0.01 mg/g wet mass decreased SOD activities by about 30-50% after 48 and 168 h compared to corresponding sham-injected values. This treatment resulted in transient oxidative stress. Lipid peroxide content increased after DDC injection at all time points in the kidney, after 48 h in the liver and was elevated in most experimental groups in the brain. Thiobarbituric-acid reactive substances (end products of lipid peroxidation) rose within the first 48 h after injection, but returned to initial levels after 168 h. Two other indices of oxidative stress were also transiently modified: protein carbonyl levels in the brain and kidney increased 24h post-injection, and the low-molecular mass thiol content was reduced over the same period in all tissues examined. Activities of catalase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase, and glucose-6-phosphate dehydrogenase showed differential responses to DDC treatment that rebounded by 168 h post-injection. Glutathione peroxidase activities were reduced by 60, 45 and 65% in the brain, liver and kidney, respectively, after 24h but rebounded thereafter. After 48 h post-injection with DDC significant decreases were also seen in liver and kidney catalase, GST activities in all three tissues, and kidney GR and G6PDH activities. In some cases, catalase, GST, GR and G6PDH activities transiently increased after 24 h. It was concluded that DDC injection depleted SOD and simultaneously stimulated lipid peroxidation, but did not require compensatory enhancement of other enzymatic defenses. Different actions of the superoxide anion in cellular metabolism and possible consequences of the impairment of superoxide dismutase are discussed.     

Exposure to tebuconazol in rice field and laboratory conditions induces oxidative stress in carp (Cyprinus carpio)

Pesticides can have an effect on the biochemical and physiological functions of living organisms. The changes seen in fish and their response to pesticides can be used as an example for vertebrate toxicity. In this study, carp fish (Cyprinus carpio) were exposed to different concentrations of tebuconazol fungicide, by rice field (31.95 μg/L) and laboratory (33.47 and 36.23 μg/L) conditional testing, during a 7 day period. Parameters such thiobarbituric acid-reactive substance levels (TBARS), protein carbonyl, catalase, glutathione S-transferase and acetylcholinesterase activities were studied, using the liver, brain and white muscle of the fish. The field experiment showed that the TBARS levels were increased in all the analyzed tissues. Similarly, the protein carbonyl of the liver and the brain AChE activity increased after 7 days. The laboratory experiment demonstrated that the TBARS levels in the liver were increased in both of the concentration tests. TBARS levels in the muscle increased only by the lowest test concentration. On the other hand, the protein carbonyl was increased only by the highest concentration. The results indicate that the tebuconazol exposure from the field and laboratory conditions directly affected the health of the fish, showing the occurrence of oxidative stress.     

Impact of Hemidesmus indicus R.Br. extract on ethanol-mediated oxidative damage in rat kidney

The antioxidant effect of the ethanolic extract of Hemidesmus indicus R.Br. root (EHI), an indigenous Ayurvedic medicinal plant in India, was studied in rats with ethanol-induced nephrotoxicity. Administering 5 g/kg body weight/day of ethanol for 60 days to male Wistar rats resulted in significantly elevated levels of serum urea, creatinine and uric acid as well as kidney thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LOOH) and conjugated dienes (CD) as compared to those of the experimental control rats. Decreased levels of kidney superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH), vitamin C and vitamin E were also observed on alcohol administration as compared with those of the experimental control rats. EHI was administered at a dose of 500 mg/kg body weight/day for the last 30 days of the experiment to rats with ethanol-induced kidney injury, which significantly decreased the levels of serum urea, uric acid and creatinine as well as kidney TBARS, LOOH and CD and significantly elevated the activities of SOD, CAT, GPx, GSH, vitamin C and vitamin E in kidney as compared to that of untreated ethanol-administered rats. Histopathological observations also correlated with the biochemical parameters. Thus, the data indicate that treatment with EHI offers protection against free radical-mediated oxidative stress in kidney of animals with ethanol-induced nephrotoxicity.     

The regulation of heat shock proteins in response to dehydration in <Emphasis Type="Italic">Xenopus laevis</Emphasis>

African clawed frogs (Xenopus laevis) endure bouts of severe drought in their natural habitats and survive the loss of approximately 30% of total body water due to dehydration. To investigate molecular mechanisms employed by X. laevis during periods of dehydration, the heat shock protein response, a vital component of the cytoprotective stress response, was characterized. Using western immunoblotting and multiplex technology, the protein levels of HSP27, HSP40, HSP60, HSP70, HSC70, and HSP90 were quantified in the liver, skeletal muscle, kidney, lung, and testes from control frogs and those that underwent medium or high dehydration (~16 or ~30% loss of total body water). Dehydration increased HSP27 (1.45–1.65-fold) in the kidneys and lungs, and HSP40 (1.39–2.50-fold) in the liver, testes, and skeletal muscle. HSP60 decreased in response to dehydration (0.43–0.64 of control) in the kidneys and lungs. HSP70 increased in the liver, lungs, and testes (1.39–1.70-fold) during dehydration, but had a dynamic response in the kidneys (levels increased 1.57-fold with medium dehydration, but decreased to 0.56 of control during high dehydration). HSC70 increased in the liver and kidneys (1.20–1.36-fold), but decreased in skeletal muscle (0.27–0.55 of control) during dehydration. Lastly, HSP90 was reduced in the kidney, lung, and skeletal muscle (0.39–0.69 of control) in response to dehydration, but rose in the testes (1.30-fold). Overall, the results suggest a dynamic tissue-specific heat shock protein response to whole body dehydration in X. laevis.     

Impact of Hemidesmus indicus R.Br. extract on ethanol-mediated oxidative damage in rat kidney

Abstract

The antioxidant effect of the ethanolic extract of Hemidesmus indicus R.Br. root (EHI), an indigenous Ayurvedic medicinal plant in India, was studied in rats with ethanol-induced nephrotoxicity. Administering 5 g/kg body weight/day of ethanol for 60 days to male Wistar rats resulted in significantly elevated levels of serum urea, creatinine and uric acid as well as kidney thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LOOH) and conjugated dienes (CD) as compared to those of the experimental control rats. Decreased levels of kidney superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH), vitamin C and vitamin E were also observed on alcohol administration as compared with those of the experimental control rats. EHI was administered at a dose of 500 mg/kg body weight/day for the last 30 days of the experiment to rats with ethanol-induced kidney injury, which significantly decreased the levels of serum urea, uric acid and creatinine as well as kidney TBARS, LOOH and CD and significantly elevated the activities of SOD, CAT, GPx, GSH, vitamin C and vitamin E in kidney as compared to that of untreated ethanol-administered rats. Histopathological observations also correlated with the biochemical parameters. Thus, the data indicate that treatment with EHI offers protection against free radical-mediated oxidative stress in kidney of animals with ethanol-induced nephtrotoxicity.     

Acute effects of glyphosate herbicide on metabolic and enzymatic parameters of silver catfish (Rhamdia quelen)

Silver catfish (Rhamdia quelen; Teleostei) were exposed to commercial formulation Roundup, a glyphosate herbicide: 0 (control), 0.2 or 0.4 mg/L for 96 h. Fish exposed to glyphosate showed an increase in hepatic glycogen, but a reduction in muscle glycogen at both concentrations tested. Glucose decreased in liver and increased in muscle of fish at both herbicide concentrations. Glyphosate exposure increased lactate levels in liver and white muscle at both concentrations. Protein levels increased in liver and decreased in white muscle while levels of ammonia in both tissues increased in fish at both glyphosate concentrations. Specific AChE activity was reduced in brain after treatments, no changes were observed in muscle tissue. Catalase activity in liver did not change during of exposure. Fish exposed to glyphosate demonstrated increased TBARS production in muscle tissue at both concentrations tested. For both glyphosate concentrations tested brain showed a reduction of TBARS after 96 h of exposure. The present results showed that in 96 h, glyphosate changed AChE activity, metabolic parameters and TBARS production. The parameters measured can be used as herbicide toxicity indicators considering environmentally relevant concentration.     

Indices of oxidative stress. 2. Lipid peroxides

Two methods of the determination of lipid peroxidation products have been compared which are based on Fe(II) oxidation by them at acid pH values in the presence of xylenol orange which binds Fe(III) have been compared. The first method uses cumene hydropeoxide as an internal standard. In the second one, lipid peroxides are previously reduced by triphenylphosphine and these substances content is measured as a difference of the production of complexes with xylenol orange and iron ions in the control (with reduction) and experimental sample (without reduction). The optimization of measurement conditions is described. The levels of lipid peroxides in goldfish tissues assayed simultaneously by two methods were similar. The method with cumene hydroperoxide needs less amounts of biological material; moreover, there is no necessity in a calibration curve. Effects of hyperoxia on lipid peroxide levels in goldfish tissues were studied with the cumene method. Within the first hours of hyperoxia this index increased 13-times in the liver and 2-times in the brain and muscle. The further exposure rebounded this parameter to the initial level. Levels of lipid peroxides positively correlated with levels of end products of lipid peroxidation (thiobarbiturate acid reactive substances) in the goldfish tissues. The method of quantification of lipid peroxides with cumene is recommended for wide using in biological investigations.     

Acute heat stress induces oxidative stress in broiler chickens

The stress responses and possible oxidative damage in plasma, liver and heart were investigated in broiler chickens acutely exposed to high temperature. Eighty 5-week old broiler chickens were exposed to 32 degrees C for 6h. The extent of lipid peroxidation, activities of superoxide dismutase and total antioxidant power in plasma, liver and heart tissues were investigated. Meanwhile, the blood metabolites such as glucose, urate, triiodothyronine, thyroxine, corticosterone, ceruloplasmin and creatine kinase were measured before and after 3 and 6h of heat exposure. The results showed that oxidative stress could be induced in 5-week old broiler chickens by acute heat exposure (32 degrees C, 6h). The results suggest that the elevated body temperature can induce the metabolic changes that are involved in the induction of oxidative stress. The liver is more susceptible to oxidative stress than heart during acute heat exposure in broiler chickens. The oxidative stress should be considered as part of the stress response of broiler chickens to heat exposure.     

Differential expression pattern of heat shock protein 70 gene in tissues and heat stress phenotypes in goats during peak heat stress period

It has been established that the synthesis of heat shock protein 70 (Hsp70) is temperature-dependent. The Hsp70 response is considered as a cellular thermometer in response to heat stress and other stimuli. The variation in Hsp70 gene expression has been positively correlated with thermotolerance in Drosophila melanogaster, Caenorhabditis elegans, rodents and human. Goats have a wide range of ecological adaptability due to their anatomical and physiological characteristics; however, the productivity of the individual declines during thermal stress. The present study was carried out to analyze the expression of heat shock proteins in different tissues and to contrast heat stress phenotypes in response to chronic heat stress. The investigation has been carried out in Jamunapari, Barbari, Jakhrana and Sirohi goats. These breeds differ in size, coat colour and production performance. The heat stress assessment in goats was carried out at a temperature humidity index (THI) ranging from 85.36–89.80 over the period. Phenotyping for heat stress susceptibility was carried out by combining respiration rate (RR) and heart rate (HR). Based on the distribution of RR and HR over the breeds in the population, individual animals were recognized as heat stress-susceptible (HSS) and heat stress-tolerant (HST). Based on their physiological responses, the selected animals were slaughtered for tissue collection during peak heat stress periods. The tissue samples from different organs such as liver, spleen, heart, testis, brain and lungs were collected and stored at ?70 °C for future use. Hsp70 concentrations were analyzed from tissue extract with ELISA. mRNA expression levels were evaluated using the SYBR green method. Kidney, liver and heart had 1.5–2.0-fold higher Hsp70 concentrations as compared to other organs in the tissue extracts. Similarly, the gene expression pattern of Hsp70 in different organs indicated that the liver, spleen, brain and kidney exhibited 5.94, 4.96, 5.29 and 2.63-fold higher expression than control. Liver and brain tissues showed the highest gene expression at mRNA levels as compared to kidney, spleen and heart. HST individuals had higher levels of mRNA level expression than HSS individuals in all breeds. The Sirohi breed showed the highest (6.3-fold) mRNA expression levels as compared to the other three breeds, indicating the better heat stress regulation activity in the breed.     

Metabolic recovery in goldfish: A comparison of recovery from severe hypoxia exposure and exhaustive exercise

Severe hypoxia exposure and exhaustive exercise in goldfish both elicit a strong activation of substrate-level phosphorylation with the majority of the metabolic perturbations occurring in the white muscle. Approximately half of the muscle glycogen breakdown observed during severe hypoxia exposure was accounted for by ethanol production and loss to the environment, which limited the extent of muscle glycogen recovery when animals were returned to normoxic conditions. Ethanol production in goldfish is not solely a response to anoxia/hypoxia exposure however, as a transient increase in ethanol production was observed during the early stages of recovery from exhaustive exercise. These data suggest that ethanol production is a ubiquitous "anaerobic" end product, which accumulates whenever metabolic demands exceed mitochondrial oxidative potential. Exhaustive exercise and hypoxia exposure both caused a 7 to 8 micromol g(-1) wet mass increase in muscle [lactate] and the rates of recovery following these perturbations were similar. The rates of muscle PCr and pHi recovery after hypoxia exposure and exhaustive exercise were similar with levels returning to controls values within 0.5 h. Surprisingly, liver [glycogen] was not depleted during exposure to severe hypoxia, however, during recovery from both hypoxia and exercise dramatically different responses in liver [glycogen] were noted. During the early stages of recovery, liver [glycogen] transiently increased to high levels after exhaustive exercise, while during recovery from hypoxia there was a transient decrease in liver glycogen over the same time frame. Overall, this points to the liver playing a dramatically different role in facilitating recovery from exercise compared with hypoxia exposure.     

The interactive effect of elevated temperature on deltamethrin-induced biochemical stress responses in Channa punctata Bloch

There are reports showing interactive effect of environmental factors with the toxic outcome of chemicals. We studied the interactive effect of elevated temperature as an abiotic stressor on deltamethrin-induced biochemical stress responses in a freshwater fish, Channa punctata Bloch. Heat stress (∼12 °C above ambient temperature for 3 h) and pesticide exposure (deltamethrin 0.75 ppb for 48 h) showed significant induction of heat shock protein-70 (HSP70) in liver, kidney and gills of fishes. Elevated temperature when followed by deltamethrin exposure showed synergistic effect showing a high level of HSP70 in liver and gills whereas response in the kidney was opposite. On the contrary, when deltamethrin exposure followed the heat stress, no significant difference was observed. Protein carbonylation was found to be more pronounced in heat-stressed group compared with control fish group. A significant increase in lipid peroxidation (LPO) was observed in different tissues of fish exposed to either of the stressors. In the kidney of fish exposed to heat stress followed by deltamethrin, LPO was relatively lower as compared to other treatments. Thiols content such as reduced glutathione (GSH), total thiols (T-SH), non-protein thiols (NP-SH) and protein thiols (P-SH) showed no consistent pattern in different tissues. In deltamethrin-exposed group that was subsequently exposed to heat stress, the GSH content was higher in liver and lower in both kidney and gills when compared with other groups. Alteration in the activities of antioxidant enzymes such as catalase (CAT), glutathione S-transferase (GST), glutathione reductase (GR) and glutathione peroxidase (GPx) was also observed when fish were exposed to heat stress and/or deltamethrin. Our study demonstrated that heat stress modulated biochemical stress responses in fish showing a tissue specific pattern. This implies that fish has the capacity to elicit differential response to exposure to abiotic stressors in order to reduce the systemic magnitude of stress which may otherwise lead to severe dysfunction of vital tissues.     

低温对黑线仓鼠能量代谢、抗氧化能力和氧化应激的影响

为探讨低温对机体能量代谢、器官/组织抗氧化能力和过氧化自由基水平的影响及其内在联系,本研究测定了不同时间低温和梯度低温处理的黑线仓鼠的摄食量、体重、主要内脏器官/组织的过氧化物歧化酶（SOD）、过氧化氢酶（CAT）、H₂O₂和丙二醛（MDA）水平。低温使摄食量显著增加,但未影响体重。低温暴露42 d使心脏和骨骼肌MDA水平、骨骼肌SOD活性显著升高;梯度低温使脑和肾脏H₂O₂水平、肝脏和骨骼肌SOD活性显著降低,使脑、肝脏、肺、肾脏MDA水平、脑和小肠SOD活性显著升高。抗氧化能力和过氧化自由基水平在不同器官之间相关性存在差异,同一器官内二者的相关性在肾脏为100%,肝脏66.7%,骨骼肌50.0%。结果表明：（1）过氧化自由基的产生与低温暴露的时间和程度有关;（2）不同器官/组织过氧化自由基水平不同;（3）部分器官/组织抗氧化酶活性的变化与过氧化自由基水平的变化密切相关,可能是防止过氧化损伤的主要防御系统。