Comparative studies on carbofuran-induced changes in some cytoplasmic and mitochondrial enzymes and proteins of epigeic, anecic and endogeic earthworms

Exposure of epigeic (Perionyx sansibaricus), anecic (Lampito mauritii) and endogeic (Metaphire posthuma) earthworms to four different concentrations (10 ppm, 20 ppm, 40 ppm and 80 ppm) of carbofuran for 16 days induced specific activities of cytoplasmic malate dehydrogenase (cMDH), mitochondrial malate dehydrogenase (mMDH) and lactate dehydrogenase (LDH). P. sansibaricus showed 33-52% increase in specific activities of aerobic (cMDH, mMDH) and anaerobic (LDH) enzymes and proteins (cytoplasmic and mitochondrial). In L. mauritii, the enhancement in enzyme and protein level was 30-46%. Similarly, M. posthuma indicated 29-43% increase in profile of enzymes and proteins. The significant increase was observed on 2nd or 3rd day and it was maximum on 16th day of carbofuran exposure. Maximum effect of carbofuran was on epigeic earthworm. The sensitivity of mitochondrial dehydrogenase and protein of different earthworm species to carbofuran appears to be associated with oxygen availability in different strata of soil habitats. Inductions in enzyme specific activity and protein content were concentration and time-dependent. The effect was more pronounced on aerobic enzymes (cMDH, mMDH) as compared to anaerobic (LDH) one. The increases in mitochondrial enzyme (47%) and protein (43%) were more than the cytoplasmic enzymes (35%) and protein (31%), which suggest a greater effect of carbofuran on respiratory metabolism of earthworms. The carbofuran-dependent increase in cytoplasmic and mitochondrial enzymes and proteins might be due to increased synthesis of metabolic enzymes and stress proteins.     

In vivo biochemical changes in liver and gill of Clarias batrachus during cypermethrin exposure and following cessation of exposure

The sublethal effect of a synthetic pyrethroid, cypermethrin on total protein, amino acids, ammonia, glycogen, and enzymes like aminotransaminases (AIAT, AAT), glutamate dehydrogenase, and glycogen phosphorylases (a and ab) was studied in physiological important tissues viz; liver and gill tissues of freshwater teleost air breathing fish, Clarias batrachus. The study was conducted during exposure of 1/3 (33%) of LC₅₀ concentration and followed by cessation of exposure. Thirty-six fish were exposed to 0.07 mg/L cypermethrin for 10 days. After 10 days, 18 fish were released to freshwater and kept in the same for 10 days (recovery group). Thirty-six fish were kept in freshwater as control batch. Protein content in liver tissues decreased at the end of 1st and 5th day followed by slight increase at the end of 10th day. Gill tissue showed statistical significant decrease (P < 0.001) in protein content during exposure period of 10 days. Recovery in protein content was observed to a large extent in both the tissues. Total free amino acids were increased in liver and gill tissues throughout the treatment period, recovery response was seen after cessation of exposure. Ammonia level was decrease in both the tissues throughout the exposure period except in liver tissue at the end of 1st day of exposure. Recovery response was exhibited by both the tissues. A decreased in glycogen content of liver tissue was observed during exposure period, gill tissue also showed decrease in glycogen at the end of 1st and 5th day followed by increase at the end of 10th day of exposure period. When the fish were transferred to freshwater, recovery in glycogen content was noted. The activity level of alanine, aspartate aminotransaminase, glutamate dehydrogenase, and phosphorylases (a, ab) was increased in both the tissues, followed by recovery response after released of fish into freshwater. The present study showed that cypermethrin caused alterations in certain biochemical mechanisms of C. batrachus. This fish indicated recovery response when transferred to cypermethrin free water.     

Influence of Atrazine and Roundup pesticides on biochemical and molecular aspects of Biomphalaria alexandrina snails

The excessive use of pesticides in agriculture has sparkled the interest of scientists in investigating the harmful effects of these compounds. The present study evaluates the pesticides Atrazine and Roundup (glyphosate) on biochemical and molecular aspects of Biomphalaria alexandrina snails. The results showed that LC₁₀ of these two pesticides caused considerable reduction in survival rates and egg production of treated snails. Additionally, Atrazine proved to be more toxic to B. alexandrina snails than Roundup. In treated snails, glucose concentration (GL) in the hemolymph as well as lactate (LT) and free amino acid (FAA) in soft tissues of treated snails increased while glycogen (GN), pyruvate (PV), total protein (TP), nucleic acids (DNA and RNA) levels in snail’s tissues decreased. The activities of glycogen phosphorylase (GP), superoxide dismutase (SOD), catalase (CAT) and glutathione reductase (GR), succinic dehydrogenase (SDH), acetylcholinesterase (AChE), lactic dehydrogenase (LDH) and phosphatases (ACP and ALP) enzymes in homogenate of snail’s tissues were reduced in response to the treatment with the two pesticides while lipid peroxide (LP) and transaminases (GOT and GPT) activity increased (P < 0.001). The changes in the number, position and intensity of DNA bands induced by pesticides may be attributed to the fact that pesticide can induce genotoxicity through DNA damage. It was concluded that the pollution of the aquatic environment by Atrazine and Roundup pesticides, would adversely affect the metabolism of the B. alexandrina snails, and have adverse effects on its reproduction.     

Impact of phorate on malate dehydrogenases, lactate dehydrogenase and proteins of epigeic, anecic and endogeic earthworms

The effects of an organophosphate pesticide phorate on cytoplasmic malate dehydrogenase (cMDH), mitochondrial malate dehydrogenase (mMDH), lactate dehydrogenase (LDH), supernatant and mitochondrial proteins of an epigeic (Perionyx sansibaricus), anecic (Lampito mauritii) and endogeic (Metaphire posthuma) earthworms were studied. The treatment of different concentrations (20, 40, 80 and 160 ppm) of phorate for 16 days gradually decreased the specific activities of cMDH, mMDH and LDH as well as cytoplasmic and mitochondrial protein contents. This showed the inhibitory effect of phorate on metabolic enzymes and proteins in tropical earthworms. The inhibition was dose- and time-dependent. The inhibitory response in mitochondrial enzyme (mMDH) and protein was somewhat earlier and more as compared to the inhibitory effect of phorate on cytoplasmic enzymes (cMDH, LDH) and protein. This indicates a greater interference of phorate in cellular respiration of earthworms. The phorate related decreases in enzyme and protein profiles were about 60% and 58% in P. sansibaricus, 54% and 49% in L. mauritii and 47% and 42% in M. posthuma, respectively. It reflects phorate-induced substantial decline in protein synthesis and aerobic and anaerobic capacity of earthworms. The maximum effect of phorate was on epigeic earthworm followed by anecic and endogeic species. The present findings suggest the differential sensitivity of different earthworm species in enzymatic and protein responses to phorate and the sensitivity was associated with the ecophysiological categories of earthworms.     

Toxic effects of novel organophosphorus insecticide (RPR-V) on certain biochemical parameters of euryhaline fish, Oreochromis mossambicus

The euryhaline fish, Oreochromis mossambicus was exposed to sub-lethal concentration (0.017 mg L⁻¹) of a novel phosphorothionate, 2-butenoic acid-3-(diethoxy phosphinothionyl) ethyl ester (RPR-V) for 30 days and allowed to recover for 7 days. Important biomarker enzymes were assayed in plasma, brain, gill, liver, kidney, and muscle during exposure tenures of day-3, -7, -15, -30, and also at 7 days (withdrawal) after stopping treatment. Acetylcholinesterase (AChE) activities of brain, gill, and muscle were strongly inhibited by 67, 75, and 66%, respectively, on day-30. Exposure (time) dependent increases in alanine aminotransferase (ALAT), and aspartate aminotransferase (ASAT), acid phosphatase (AcP), and alkaline phosphatase (AkP), activities in plasma and kidney; AcP and AkP activities in gill were noticed. However, significant decrease in ALAT, ASAT, AcP, and AkP activities in liver was observed. The depletion of glycogen was observed in liver, brain, and gill tissues, an indication of typical stress related response of the fish with pesticide. A significant increase in lactate dehydrogenase (LDH) activity in gill and brain was observed and decreased in liver and muscle, indicating tissue damage and muscular harm. Depletion of glutathione (GSH) was observed in the above tissues, there by enhancing the lipid peroxidation resulting in cell damage. The induction in hepatic glutathione-S-transferase (GST) levels indicates the protection against the toxicity of xenobiotic-induced lipid peroxidation. There was a significant recovery in all the above biochemical parameters, in all the tissues of fish after a recovery period of 7 days. These results revealed that RPR-V affects the intermediary metabolism of O. mossambicus and the increase of biomarker enzymes in plasma, might be due to the necrosis of liver.     

Tissue-specific antioxidative and neurotoxic responses to diazinon in Oreochromis niloticus

The purpose of this study was to evaluate oxidative stress and neurotoxic potential of organophosphorus (OP) insecticide diazinon in the sentinel freshwater fish, Oreochromis niloticus. Antioxidant and acetylcholinesterase (AChE) enzyme activities and malondialdehyde (MDA) and protein levels were measured spectrophotometrically in gill, kidney, alimentary tract, and muscle tissues of fish treated with sub-lethal diazinon concentrations for 1, 7, 15, and 30 days. Dose-dependent inhibitions of AChE were observed in all the experimental fish. On the contrary of alimentary tract, MDA levels were elevated in kidney and muscle and gill was not affected. AChE and MDA levels intercorrelated in kidney and muscle tissues. Diazinon had increased superoxide dismutase (SOD) activities in all the tissues, while kidney was the most affected tissue. Tissue-specific alterations were observed on catalase (CAT) and glutathione peroxidase (GPx) activities; however, the activities were not changed in gill and muscle tissues for GPx and in gill, muscle, and kidney tissues for CAT. Protein levels decreased in kidney, muscle, and alimentary tract, while increased in gill and alimentary tract in 15 days. With respect to these results, diazinon has oxidative and neurotoxic potentials in O. niloticus. Observed changes with diazinon treatment were generally tissue-specific and dose-dependent.     

Glucose metabolism in hepatopancreas and gill of Lamellidens marginallis during methyl parathion toxicity

Changes in glucose metabolism were studied in hepatopancreas and gill of freshwater mussel, Lamellidens marginalis, exposed to a sublethal concentration (8 ppm) of methyl parathion. A slight decrease in glycogen and pyruvate and an increase in lactate levels were observed. An increase in phosphorylase and aldolase suggested increased formation of trioses during methyl parathion toxicity. The decrease in lactate dehydrogenase activity and increase in lactate content indicated reduced mobilization of pyruvate into the citric acid cycle. Glucose-6-phosphate dehydrogenase activity was increased, suggesting enhanced oxidation of glucose by the HMP shunt pathway. Citric acid cycle enzymes such as isocitrate, succinate, and malate dehydrogenases were found to be decreased, suggesting abnormality in mitochondrial oxidative metabolism as a consequence of methyl parathion toxicity. The decreased cytochrome c oxidase and Mg²⁺-ATPase, apart from citric acid cycle enzymes, indicated impaired energy synthesis as a result of reduced aerobic oxidation of glycose. The increase in acid and alkaline phosphatase activities suggested enhanced breakdown of phosphate to release energy in view of inhibition of the ATPase system during methyl parathion stress. The changes were more pronounced in hepatopancreas as compared to gill of mussel exposed to methyl parathion.     

Mechanism of fenvalerate-withdrawal-dependent recovery in metabolism of a catfish, Clarias batrachus

The effects of protein synthesis inhibitors on fenvalerate-withdrawal-dependent recovery in citrate synthase (CS), glucose 6-phosphate dehydrogenase (G6-PDH), lactate dehydrogenase (LDH), RNA, and protein of brain, liver, and skeletal muscle of Clarias batrachus were studied to explore possible mode of action of a pyrethroid insecticide at metabolic level. The administration of actinomycin D or cycloheximide inhibited partially or completely the withdrawal-dependent increase in enzyme activities, RNA, and protein contents, substantiating de novo synthesis of these macromolecules during recovery. The inhibition was more pronounced in response to cycloheximide reflecting recovery in translation process. This also suggests the possibility of fenvalerate-induced impairment of metabolism through inhibition of enzyme synthesis.     

Some hematological,biochemical, and enzymological parameters of a fresh-water teleost fish, Channa punctatus, exposed to sublethal concentrations of quinalphos

Alterations in the levels of hemoglobin, total plasma proteins, glucose, and lactic acid in the blood; glycogen and lactic acid content of liver and white skeletal muscle; and the activities of lactate dehydrogenase, pyruvate dehydrogenase, and succinate dehydrogenase in liver, kidney, intestine, brain, gills, and muscles were examined in the fresh-water snake-head fish, Channa punctatus, after exposure to a sublethal concentration (25 μg/liter) of quinalphos for 60 and 120 days. Hemoglobin, plasma protein, glucose, and lactic acid decreased in pesticide-exposed fish. The glycogen content of the liver and muscles increased but lactic acid decreased. Lactate dehydrogenase activity decreased in all six tissues. Pyruvate dehydrogenase activity of liver, kidney, gill, and muscle decreased, but the enzyme activity was elevated in intestine and brain. In intestine, succinate dehydrogenase activity was elevated, and in the remaining five tissues the enzyme activity was significantly reduced. The present study showed that formation of glycogen and its breakdown was impaired in the liver, and aerobic oxidation of nutrients was adversely affected in quinalphos-exposed fish.     

Determination of toxicity of trichloroacetic acid in rats: 50 days drinking water study

This study aims to investigate the effects of the trichloroacetic acid (TCA) on serum marker enzymes [aspartate aminotransferase (AST), alanin aminotransferase (ALT), creatine phosphokinase (CPK), acid phosphatase (ACP), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH)], antioxidant defense systems [Reduced glutathione (GSH), glutathione reductase (GR), superoxide dismutase (SOD), glutathione-S-transferase (GST) and catalase (CAT)] and lipid peroxidation content (Malondialdehyde, MDA) in various tissues of rats. TCA (2000 ppm) as drinking water was administered orally to rats (Sprague-Dawley albino) ad libitum for 50 days continuously. TCA treatments caused different effects on the serum marker enzymes, antioxidant defense systems and the MDA content in experimented rats compared to controls. Results showed that TCA caused a significant increase in serum AST, ALT, CPK and ACP activity. The lipid peroxidation end product MDA slightly increased in the erythrocytes, liver and kidney of rats treated with TCA, whereas did not change in the brain. In addition, antioxidant enzyme activity such as CAT and SOD significantly increased in the brain, liver and kidney tissues of TCA induced group whereas the ancillary enzyme GR and the drug metabolizing enzyme GST activity did not significantly change in the all tissues. The observations presented led us to conclude that the administration of subchronic TCA promotes lipid peroxidation content, elevates tissue damage serum marker enzymes and fluctuates in the antioxidative systems in rats. Also the rats resisted to oxidative stress via antioxidant mechanism but the antioxidant mechanism could not prevent the increases in lipid peroxidation in rat’s tissues. These data, along with the determined changes suggest that TCA produced substantial systemic organ toxicity in the erythrocyte, liver, brain and kidney during the period of a 50-day subchronic exposure.     

Ecophysiological category based toxicological responses in metabolism of earthworms: Impact of a pyrethroidal insecticide

Effects of alphamethrin (0.04 ppm, 0.08 ppm, 0.16 ppm, 0.32 ppm) on some metabolic dehydrogenases and proteins for 1, 2, 3, 4, 8 and 16 days using three ecologically different earthworm species (Perionyx sansibaricus, Lampito mauritii and Metaphire posthuma) were studied. The first significant effect was on 2nd/3rd day and maximum response was achieved on 16th day of exposure of alphamethrin at all concentrations. Similarly, maximum effect was obtained at 0.32 ppm alphamethrin at different exposure periods. It showed a dose- and duration-dependent inhibitory effects of a pyrethroid on enzymes and proteins of earthworms. There were approximately 47%, 43% and 41% declines in specific activities of cytoplasmic malate dehydrogenase (cMDH) of P. sansibaricus, L. mauritii and M. posthuma, respectively, in response to 0.32 ppm exposure of alphamethrin for 16 days. In case of similar treatment, specific activities of mitochondrial malate dehydrogenase (mMDH) showed 57%, 51% and 45% reductions in epigeic (P. sansibaricus), anecic (L. mauritii) and endogeic (M. posthuma) earthworms, respectively. Exposure of alphamethrin (0.32 ppm) also decreased the specific activities of lactate dehydrogenase (LDH) by 47% (P. sansibaricus), 35% (L. mauritii) and 39% (M. posthuma) in different types of earthworms. The reductions in specific activities of a Krebs cycle enzyme (mMDH) were greater than that of a glycolytic enzyme (LDH). The protein contents declined significantly in the earthworms exposed to alphamethrin. The decreases of 41%, 36% and 30% were obtained in cytoplasmic proteins of P. sansibaricus, L. mauritii and M. posthuma, respectively. However, the mitochondrial proteins showed reductions of 45% in P. sansibaricus, 46% in L. mauritii and 38% in M. posthuma in response to alphamethrin (0.32 ppm) intoxication for 16 days. The decrease in the protein content reflected an inhibitory effect of alphamethrin on protein turnover. The most pronounced effect of alphamethrin was on metabolic enzymes and proteins of P. sansibaricus and least effect was found on M. posthuma. This clearly showed that surface dwelling species of earthworms (epigeic) are more vulnerable to toxic chemical than deep burrowing species (endogeic). Thus a possible ecophysiological link exists between the toxicological responses and ecological categories at metabolic level in tropical earthworms.     

Amelioratory effect of vitamin E on organophosphorus insecticide diazinon-induced oxidative stress in mice liver

Considering that the involvement of reactive oxygen species (ROS) has been implicated in the toxicity of organophosphate insecticides (OPIs), the aim of this study was to investigate the ameliorative properties of vitamin E (vitE) against the subchronic effect of diazinon (DZN) on oxidative damage markers such as lipid peroxidation (LPO) and the antioxidant defense system (ADS) in the liver of male MFI albino mice. The groups were intraperitoneally (i.p) administered with either vehicle or vitE (100 mg/kg body weight) or ¼ LD₅₀ of DZN (16.25 mg/kg b.w.) or ½ LD₅₀ of DZN; 32.5 mg/kg b.w) or ¼ LD₅₀-DZN + vitE or ½ LD₅₀ + vitE every consecutive day for 14 days. Hepatic damage markers analysis revealed that alanine transferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) were significantly decreased in both DZN doses. Also, the significantly increased levels of biomarkers of oxidative stress as LPO and protein carbonyl (PC) and the decreased antioxidant defenses like reduced glutathione (GSH), and free radical scavenger enzymes viz., catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione reductase (GSH-Rx) were noted in DZN-treated groups as compared to control group. Distinctly lower levels of GSH and increased levels of LPO, along with alterations in endogenous antioxidant enzymes were evident in hepatic toxicity of DZN which is dose-dependent. Hepatic specific marker enzymes were restored to normalcy in mice supplemented with vitE following treatment with DZN which otherwise was decreased in the DZN-treated mice. The results show that co-treatment of vitE with DZN prevents or diminishes the oxidative stress of DZN-treated mice and may act as a putative protective agent against DZN-induced liver tissue injury.     

Evaluation of etoxazole toxicity in the liver of Oreochromis niloticus

The effects of etoxazole were evaluated in freshwater fish Oreochromis niloticus from five different sublethal etoxazole concentrations in order to study the biochemical response, photometrically. No changes were observed in the activities of antioxidant enzymes such as superoxide dismutase (SOD, EC 1.15.1.1), catalase (CAT, EC 1.11.1.6), and glutathione peroxidase (GPx, EC 1.11.1.9). These were measured in liver after 1, 7, and 15 days of exposure to sublethal concentrations of 0.2, 0.4, 0.6, 0.8, and 1% of field application rate (134.75 ppm). This study also investigated the levels of neurotoxic effects by the determination of acetylcholine esterase (AChE EC 3.1.1.7) and sodium-potassium adenosine 5^′-triphosphatase (Na⁺K⁺-ATPase, EC 3.6.3.9) activities. The exposure of fish led to sharp depletion in AChE activity while there is no significant alteration in Na⁺K⁺-ATPase activity. Up to 80% decreases were observed in the AChE activity. Since no difference was found in the activity of glutamate-pyruvate transaminase (GPT, EC 2.6.1.2), etoxazole did not show hepatotoxic effect. The results of the present study show that increase in the malondialdehyde (MDA) contents and decrease in the AChE activity can be used as biomarkers for monitoring toxicity in etoxazole exposure.     

Subacute oral toxicity of chlorpyriphos and protective effect of green tea extract

This paper reports the effect of green tea administration following subacute toxicity caused by exposure to organophosphorus pesticide chlorpyriphos in liver of rats. Four groups containing five male Sprague-Dawley rats each were selected. Group I served as control. Group II rats were permitted free access to solubilised crude extract of green tea (1.5%w/v in water) as the sole drinking fluid. Group III rats were given a single daily oral dose of chlorpyriphos (30 mg/kg bodyweight in corn oil). Group IV rats received oral dose of pesticide and green tea extract simultaneously. All rats were sacrificed after 15 days. Significant damage to liver was observed via increased serum levels of transaminases and alkaline phosphatase. Lipid peroxidation showed a 5-fold increase in pesticide exposed rats compared to control. In contrast, levels of antioxidant GSH, glutathione-dependent enzymes like glutathione peroxidase (GPx), glutathione S-transferase (GST) and free radical scavengers like catalase (CAT) and superoxide dismutase (SOD) were significantly lower than those of the control group reinforcing oxidative damage. The use of green tea extract appeared to be beneficial to rats, although not to a great extent in significantly reducing and reversing the damage sustained by pesticide exposure and favors recovery.     

Influence of subacute and subchronic treatment of abcisic acid and gibberellic acid on serum marker enzymes and erythrocyte and tissue antioxidant defense systems and lipid peroxidation in rats

This study describes the subacute and subchronic effects of two plant growth regulators (PGRs) [abcisic acid (ABA) and gibberellic acid (GA₃)] on serum marker enzymes [aspartate aminotransferase (AST), alanine aminotransferase (ALT), creatine phosphokinase (CPK) and lactate dehydrogenase (LDH), γ-glutamil transpeptidase (GGT)], antioxidant defense systems [reduced glutathione (GSH), glutathione reductase (GR), glutathione peroxidase (GPx), superoxide dismutase (SOD), glutathione-S-transferase (GST) and catalase (CAT)] and lipid peroxidation level (Malondialdehyde = MDA) in various tissues of rats. Rats (Sprague-Dawley albino) were exposed to 75 ppm (parts per million) of ABA and GA₃. Seventy-five parts per million of PGRs as drinking water was administered orally ad libitum for 25 and 50 days continuously. The PGRs treatments caused different effect on the serum marker enzymes, antioxidant defense systems and the content of MDA in comparison to those of control rats. Results show that ABA caused a significant decrease in serum LDH and CPK activity with both periods. Also, GA₃ significantly decreased serum AST, CPK, and LDH activity with subacute and decreased serum ALT, CPK, LDH, and GGT treated with subchronic periods. The lipid peroxidation end product MDA significantly increased in the erythrocyte, liver, brain, and muscle of rats treated with both the period of GA₃ without significantly change in the erythrocyte and muscle of rats treated with the subacute period of ABA. The GSH levels were significantly depleted in the erythrocyte and brain of rats treated with both the period of GA₃ without any change in the erythrocyte, liver, brain, and muscle of rats treated with both the period of ABA. Also GSH levels in the muscle significantly depleted with the subchronic period of GA₃. Antioxidant enzyme activities such as SOD significantly decreased in the erythrocyte, liver and brain tissues but increased in the muscle tissue of rats treated with both the periods of GA₃. Meanwhile, SOD significantly decreased in liver and brain, and increased in muscle of rats treated with both the period of ABA. While CAT significantly decreased in the all tissues of rats treated with both the period of GA₃, decreased in the liver and muscle of rats treated with both the periods of ABA too. On the other hand, the ancillary enzyme GPx and GR activity in the erythrocytes, liver, brain and muscle were either significantly depleted or not changed with two periods of PGRs. The drug metabolizing enzyme GST activity significantly decreased in the brain of rats treated with subacute period of PGRs but increased in the erythrocytes of rats treated with subacute period of GA₃. As a conclusion, ABA and GA₃ had significantly increased the activity of hepatic damage enzymes. Also the rats resisted to oxidative stress via antioxidant mechanism. However, the antioxidant mechanism could not prevent the increases in lipid peroxidation in rat’s tissues. These data, along with changes, suggest that PGRs produced substantial systemic organ toxicity in the erythrocyte, liver, brain, and muscle during the period of a 25-day subacute and 50-day subchronic exposure.     

Catalase activity as a potential vital biomarker of fish intoxication by the herbicide aminotriazole

The objective of this study was to investigate the effects of the herbicide 3-amino-1,2,4-triazole (AMT) on the activities of catalase and lactate dehydrogenase (LDH) in blood (plasma and erythrocytes) and eight solid tissues of goldfish, Carassius auratus. Injection of goldfish with AMT (0.5 mg/gww AMT in 0.9% NaCl) resulted in a significant decrease in catalase activity 24 h post-injection in most tissues investigated. In white and red muscle, kidney, heart, liver, brain and erythrocytes the activity of catalase decreased by 61%, 69%, 64%, 48%, 40%, 27% and 26%, respectively, in comparison to the values seen in animals injected with physiological saline (0.9% NaCl). However, the activity of LDH decreased only in red muscle (by 19%) after AMT injection, whereas in plasma it increased by 137%. Protein carbonyl levels, a measure of oxidative damage to proteins, did not change in plasma in goldfish injected with AMT and total hemoglobin levels in AMT-injected fish, although lower compared with uninjected controls, did not differ from values in saline-injected controls. It is proposed that catalase activity in erythrocytes and white muscle might be usefully developed as a potential marker for fish intoxication by aminotriazole and other related herbicides.     

Ameliorative effect of lycopene on antioxidant status in Cyprinus carpio during pyrethroid deltamethrin exposure

The aim of the present study was to investigate the ameliorative properties of lycopene against the toxic effects of deltamethrin (DM) by examining oxidative damage markers such as lipid peroxidation and the antioxidant defense system components in carp (Cyprinus carpio). The fish were divided into seven groups of 15 fish each and received the following treatments: Group 1, no treatment; Group 2, orally administered corn oil; Group 3, oral lycopene (10 mg/kg body weight); Group 4, exposure to 0.018 μg/L DM; Group 5, exposure to 0.018 μg/L DM plus oral administration of 10 mg/kg lycopene; Group 6, exposure to 0.036 μg/L DM; and Group 7, exposure to 0.036 μg/L DM plus oral administration of 10 mg/kg lycopene. Treatment was continued for 14 days, and at the end of this period, blood and tissue (liver, kidney, and gill) samples were collected. Levels of malondialdehyde (MDA) and reduced glutathione (GSH) as well as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were determined in blood and tissues for measurement of oxidant-antioxidant status. A significant elevation in the level of MDA, as an index of lipid peroxidation, and reductions in antioxidant enzyme activities (SOD, CAT, and GSH-Px) and low molecular weight antioxidant (GSH) levels were observed in DM-exposed fish. Treatment with lycopene attenuated the DM-induced oxidative stress by significantly decreasing the levels of MDA. In addition, lycopene significantly increased the SOD, CAT, and GSH-Px activities and the level of GSH. The present results suggest that administration of lycopene might alleviate DM-induced oxidative stress.     

Carbofuran-induced biochemical changes in Clarias batrachus

The effect of carbofuran, an organo-carbamate pesticide, upon the level of protein as well as the activity of lactate dehydrogenase (EC 1.1.1.28, LDH) was studied by exposing the teleost fish, Clarias batrachus, to different subacute con-centrations (0·01 and 0·02 mg litre^-1) for 96 h and 15 days. The results showed a drastic decrease in the protein content in different body organs of the fish. The pesticide also caused a significant decrease in the level of activity of LDH in different body tissues of the fish, the effect being more pronounced in the gills, muscle, brain and liver than in kidney and heart. The decrease in protein content and the activity of LDH in fish tissues was more marked at the higher concentration of the pesticide for the longer duration of treatment. The results suggested that carbofuran has an effect at very low concentration (compared to its LC₅₀ value) possibly at the level of protein metabolism, and also inhibits the activity of LDH, the terminal glycolytic enzyme. © 1998 SCI     

Biochemical alteration induced by monocrotophos in the blood plasma of fish, Channa punctatus (Bloch)

Monocrotophos (MCP), commonly known as azodrin, is one of the organophosphate (OP) pesticides extensively used in agricultural practices throughout the world. Channa punctatus were exposed to sublethal concentrations (0.96 and 1.86 mg/L) of monocrotophos for 15 and 60 days to assess the alterations in the level of some biochemical parameters in blood plasma. Significant alterations in all the biochemical parameters were found to be dose dependent. Hypoglycemia and hypocholesteremia were observed in plasma of fish at both exposure periods (15 and 60 days). Increased activities of glutamate-oxalacetate transaminase (GOT), glutamate-pyruvate transaminase (GPT), acid and alkaline phosphatase of blood plasma indicated hepatic tissue damage. Decrease in lactate dehydrogenase (LDH) content in plasma further indicated lower metabolic rate after 60 days of exposure. Significant decline in triglycerides content was observed in fish exposed to both sublethal concentrations of monocrotophos. We suggest that analysis of biochemical parameters in the fish blood may be useful in environmental biomonitoring.     

Impact of sodium cyanide on catalase activity in the freshwater exotic carp, Cyprinus carpio (Linnaeus)

The Cyprinus carpio fingerlings on exposure to lethal (1 mg/L) and sub lethal concentrations (0.066 mg/L) of sodium cyanide showed inhibition in the activity of catalase. The disruption of catalase activity in freshwater fish, C. carpio is demonstrated in the present study using UV–visible spectrophotometer at 240 nm using hydrogen peroxide as a substrate. It suggests toxic effects of sodium cyanide and consequent accumulation of hydrogen peroxide in the functionally different tissues namely, liver, gill, muscle and brain. This might lead to cellular damages, and create widespread physiological disturbance. The results suggest that catalase activity can be a good diagnostic tool for sodium cyanide toxicity in biomonitoring programme.