Chronic effects of mercuric chloride on the activities of some enzymes in certain tissues of the fresh water murrel, Channapunctatus

Alterations in the activities of some enzymes in the brain, gills, intestine, kidney, liver and muscles have been examined in the fresh water murrel, $\text{Channa}$$\text{punctatus}$, after exposure to a sublethal concentration of mercuric chloride (3 μg/1) for 15, 30 and 60 days. The results revealed that after 15 days of exposure amino acid oxidase activity was elevated in brain and liver and inhibited in intestine. The activity of xanthine oxidase was increased in gills, and inhibited in kidney. Thirty days exposure produced significant inhibition in the activities of malate dehydrogenase in liver, glutamate dehydrogenase in gills and brain, aminoacid oxidase in gills, and xanthine oxidase in liver and intestine. In contrast, glutamate dehydrogenase in intestine, kidney and liver and aminoacid oxidase in brain and liver were elevated. After 60 days of treatment, a decrease in the activity of glucose-6-phosphatase was recorded in gills, intestine, kidney and liver. Hexokinase activity in kidney and liver, and malate dehydrogenase in all the six tissues were inhibited. Glutamate dehydrogenase activity in intestine, kidney and liver remained higher than in control fish. In brain, kidney and liver the activity of aminoacid oxidase was elevated, but in gills the enzyme activity decreased. Xanthine oxidase activity was inhibited in intestine and liver.     

Alteration in some biochemical and enzymological parameters in the snake head fish , exposed chronically to quinalphos

The effect of chronic quinalphos exposure (0.025 mg/1) for 15 and 30 days on the levels of glucose, lactic acid and haemoglobin in the blood; glycogen and lactic acid contents of the liver and muscles; and the activities of hexokinase, lactate dehydrogenase, pyruvate dehydrogenase and succinate dehydrogenase in liver, kidney, intestine, brain, gills and muscles was examined. Blood glucose, lactic acid and haemoglobin levels decreased in quinalphos exposed fish. Glycogen content of liver and muscles increased but lactic acid decreased. Hexokinase was inhibited in intestine and muscles after 30 days of exposure but increase in enzyme activity was noted in gills. Lactate dehydrogenase activity was inhibited in all the six tissues. Pyruvate dehydrogenase activity of liver, kidney, gills and muscles was inhibited. However, in brain the enzyme activity was elevated. Succinate dehydrogenase activity was elevated in intestine and inhibited in other tissues.     

Alteration in some biochemical and enzymological parameters in the snake head fish Channapunctatus, exposed chronically to quinalphos

The effect of chronic quinalphos exposure (0.025 mg/1) for 15 and 30 days on the levels of glucose, lactic acid and haemoglobin in the blood; glycogen and lactic acid contents of the liver and muscles; and the activities of hexokinase, lactate dehydrogenase, pyruvate dehydrogenase and succinate dehydrogenase in liver, kidney, intestine, brain, gills and muscles was examined. Blood glucose, lactic acid and haemoglobin levels decreased in quinalphos exposed fish. Glycogen content of liver and muscles increased but lactic acid decreased. Hexokinase was inhibited in intestine and muscles after 30 days of exposure but increase in enzyme activity was noted in gills. Lactate dehydrogenase activity was inhibited in all the six tissues. Pyruvate dehydrogenase activity of liver, kidney, gills and muscles was inhibited. However, in brain the enzyme activity was elevated. Succinate dehydrogenase activity was elevated in intestine and inhibited in other tissues.     

Biomarkers assessment in juvenile Cyprinus carpio exposed to waterborne cadmium

The impact of long-term exposure to waterborne cadmium (Cd) on Cyprinus carpio was evaluated through changes of selected parameters considered as biomarkers of toxicity. Fish were exposed to 1.6 mg l(-1) Cd for 14 days and then transferred to Cd-free water for 19 days. The measured parameters were gill ATPases, brain acetylcholinesterase (AchE), liver glutamate oxaloacetate (GOT) and glutamate pyruvate (GPT) transaminases, muscle water content, and protein content of liver, gills and brain. Condition factor and liver somatic index were also calculated. Branchial ATPase activities were impaired in a dissimilar way: the (Na(+),K(+))-ATPases were inhibited by approximately 30%, while the Mg(2+)-ATPase was significantly activated by 70%. Brain AchE showed no changes after Cd exposure. Both liver GOT and GPT activities were increased by the metal by 63 and 98%. Water content of the skeletal muscle showed no significant alterations. After the 19-day recovery phase, changes in the Mg(2+)-ATPase and GPT were reversed to values similar to controls, but the Cd exposure resulted in an irreversible alteration in GOT activity. Results indicate that the sublethal Cd concentrations are stressful to carp, particularly with reference to branchial enzymes which may disrupt the osmotic and ionic balance of the animals.     

Comparision of the waterborne and dietary routes of exposure on the effects of Benzo(a)pyrene on biotransformation pathways in Nile tilapia (Oreochromis niloticus)

BaP is one of the most studied PAH, due to its ubiquitous presence in aquatic environments and toxicity to aquatic organisms. The main goal of this study was to assess BaP effects in Nile Tilapia after waterborne and dietary exposures, through the evaluation of EROD and GST activities in liver, gills and intestine, and BaP metabolites in bile; and also to evaluate the usefulness of these commonly used biomarkers after two different routes of exposure. Waterborne exposure to BaP led to a significant induction of EROD in all tissues analyzed (644%, 1640% and 2880% in relation to solvent in liver, gill and intestine respectively) while in dietary exposures EROD was induced only in intestine (3143%) after exposure to high BaP concentrations. GST activities with CDNB were slightly induced in liver (40%) and in gill (66%) after water exposure to BaP, and in intestine after dietary exposure to low BaP concentrations (182%). BaP metabolites in bile increased after both exposure routes, and were highly correlated with EROD activity after water exposure. In summary, this work has shown that the effects of BaP on biotransformation pathways depend on the route of exposure. Moreover, barrier tissues like gills and intestine also have an important role in the first-pass metabolism of BaP, reducing the amount of parent compound that reaches the liver to be metabolized. For that reason, EROD activity as a biomarker of exposure should also be applied in extrahepatic organs, like gills and intestine, in monitoring studies. Biliary BaP type metabolites are good reflectors of contamination levels under both exposure routes, while GST activity with CDNB as substrate, as a phase II enzyme, does not seem a reliable biomarker of exposure to BaP regardless the route of exposure.     

Cypermethrin induced alterations in nitrogen metabolism in freshwater fishes

In the present study, two fresh water fishes namely, Channa punctatus and Clarias batrachus, were exposed to three sub-acute concentrations of synthetic pyrethroid, cypermethrin, for 96 h to evaluate the role of amino acids in fulfilling the immediate energy needs of fishes under pyrethroid induced stress as well as to find out the mechanism of ammonia detoxification. The experiments were designed to estimate the levels of free amino acid, urea, ammonia and the activities of aspartate aminotransferase (AAT), alanine aminotransferase (AlAT), glutamate dehydrogenase (GDH), glutamine synthetase (GS) and arginase in some of the vital organs like brain, gills, liver, kidney and muscle of both fish species. The significant decrease in the levels of amino acids concomitant with remarkable increase in the activities of AAT, AlAT and GDH in these vital tissues of fish species elucidated the amino acid catabolism as one of the main mechanism of meeting out the immediate energy demand of the fishes in condition of cypermethrin exposure. The levels of ammonia were significantly increased at 10% of 96 h LC(50) of cypermethrin in the different organs such as brain, gills, liver, kidney and muscle of both fish species while 15% and 20% concentrations of 96 h LC(50) of cypermehrin registered remarkable decline in both fish species. The differential increment in the activities of GDH, GS and arginase and in the level of urea established three different alternative mechanisms of ammonia detoxification. The results indicated that in C. punctatus, the prevalent mode of nitrogen excretion is in the form of conversion of ammonia into glutamine and glutamate while in C. batrachus, the excessive nitrogen is excreted in the form of urea synthesized from ammonia.     

Effects of hexachlorobenzene on antioxidant status of liver and brain of common carp (Cyprinus carpio)

Hexachlorobenzene (HCB)-induced oxidative damages have been published in rats while the effects have not yet been reported in fishes. Juvenile common carps (Cyprinus carpio) were exposed to waterborne HCB from 2 to 200 microg l-1 for 5, 10 or 20 days. Liver and brain were analyzed for various parameters of oxidative stress. There were no significant changes of glutathione (GSH) content and superoxide dismutase (SOD) activity in liver after 5 or 10 days exposure, whereas obvious drops were observed at higher concentrations after 20 days exposure. Significant decreases of GSH content and SOD activity in brain were found during all the exposure days. In brain, HCB also significantly elevated the contents of reactive oxygen species (ROS), thiobarbituric acid- reactive substances (TBARS, as an indicator of lipid peroxidation products), glutathione disulfide (GSSG), and activities of nitric oxide synthase (NOS), glutathione peroxidase (GPx), and glutathione reductase (GR), and inhibited activities of acetylcholinesterase (AchE) and glutathione S-transferase (GST). The results clearly demonstrated that environmentally possible level of HCB could result in oxidative stress in fish and brain was a sensitive target organ of HCB toxicity.     

Effects of experimental terbuthylazine exposure on the cells of Dicentrarchus labrax (L.)

The effects of acute exposure to the herbicide terbuthylazine (3.55, 5.01 and 7.08 mg l(-1)) on the cells of farmed European sea bass, Dicentrarchus labrax L., were investigated by means of light and electron microscopy. In gills of treated fish, the number of chloride cells (CCs) and rodlet cells (RCs) increased significantly within 24 h and 48 h, respectively; the intestine showed the largest increase in RCs linked to treatment and exposure time. In kidney, 24 h exposure induced a significant increase in RCs and the number and global area of macrophage aggregates (MAs). Treated fish displayed cellular and/or ultrastructural alterations in all the organs examined. In the gills necrosis, lamellar and cellular oedema, epithelial lifting, telangectasia, and fusion of secondary lamellae were encountered. The liver presented myelin-like figures, cytoplasmic rarefaction and acute cell swelling of hepatocytes. In both organs, the severity of damage was dose-dependent. In RCs of gills, the intestine and kidney of exposed sea bass, high cytoplasmic vacuolization, myelin-like figures, cristolysis and varying degrees of rodlet degeneration were observed. Extensive rodlet expulsion occurred in the gut lumen. Exposure to terbuthylazine also affected the renal tubular epithelial cells, which exhibited 'blebs'. Damage to the intestinal epithelial cells was also observed.     

Cadmium accumulation and elimination in tissues of juvenile olive flounder, Paralichthys olivaceus after sub-chronic cadmium exposure

Experiments were carried out to investigate the accumulation and elimination of cadmium (Cd) in tissues (gill, intestine, kidney, liver and muscle) of juvenile olive flounder, Paralichthys olivaceus, exposed to sub-chronic concentrations (0, 10, 50, 100 microg l(-1)) of Cd. Cd exposure resulted in an increased Cd accumulation in tissues of flounder with exposure periods and concentration, and Cd accumulation in gill and liver increased linearly with the exposure time. At 20 days of Cd exposure, the order of Cd accumulation in organs was gill > intestine > liver > kidney > muscle and after 30 days of exposure, those were intestine > gill > liver > kidney > muscle. An inverse relationship was observed between the accumulation factor (AF) and the exposure level, but AF showed an increase with exposure time. During the depuration periods, Cd concentration in the gill, intestine and liver decreased immediately following the end of the exposure periods. No significant difference was found Cd in concentration in the kidney and muscle during depuration periods. The order of Cd elimination rate in organs were decreased intestine > liver > gill during depuration periods.     

Changes in the activities of some digestive enzymes of Channa punctatus, exposed chronically to mercuric chloride

The effect of a chronic exposure to sublethal concentration of mercuric chloride (0.3 mg/l) on the activities of some enzymes in the digestive system of the teleost fish Channa punctatus was examined after 15 and 30 days of treatment. Glucose-6-phosphatase was significantly inhibited in the intestine and pyloric caeca. No marked alterations were observed in the activities of maltase and lactase except for elevation in maltase activity and inhibition in lactase activity in the intestine and pyloric caeca after 15 days of treatment. Three peptidases (aminotripeptidase, glycylglycine dipeptidase and glycyl-1-leucine dipeptidase) showed decreased activities in all parts of the digestive system. A decrease was also observed in the activity of lipase except for the stomach where inhibition after 15 days was insignificant. The results indicate that the activities of all the enzymes examined are inhibited in intestine and pyloric caeca and digestion of proteins and lipids may be more affected by mercury than the digestion of some carbohydrates.     

Changes in the levels of aspartate and alanine aminotransferase activities of Anabastestudineus (Bloch) exposed to disyston

In $\text{Anabas}$$\text{testudineus}$, the per cent changes noted in the aspartate aminotransferase (AAT) activities of gill, brain, intestine, liver, muscle and kidney until 6 hr of exposure to lethal concentration (10.5 mg/L disyston) were relatively much less when compared to those of sublethal concentration (4.0 mg/L disyston). But in the case of alanine aminotransferase (AIAT) activity, the tissues which showed such effect (paradoxical effect) were gill, brain and liver.     

Adenosine triphosphatase activities in brain, kidney and liver of mice treated with toxaphene.

The sensitivity of Na+-K+ and Mg++ Adenosine Triphosphatases (ATPases) in mouse tissues to toxaphene, a highly chlorinated camphene, was determined both in vivo and in vitro. The brain and kidney Na+-K+ ATPase activities were significantly inhibited in vitro by toxaphene. Interestingly, the inhibition was not significantly increased with an increase in the concentration of toxaphene. The oligomycin-sensitive (mitochondrial Mg++ ATPase activities in mouse brain, kidney and liver fractions were significantly inhibited by toxaphene in a concentration-dependent fashion. The oligomycin-insensitive Mg++ ATPase in all tissues examined was also inhibited but less sensitive to toxaphene than mitochondrial Mg++ ATPase. In contrast to in vitro response, the brain ATPases were not altered in mice fed toxaphene by oral intubation for three days. The renal and hepatic ATPase activities were significantly decreased in toxaphene treated mice with the oligomycin-insensitive Mg++ ATPase activity being only slightly altered.     

Changes in the activities of some digestive enzymes of Channa punctatus,exposed chronically to mercuric chloride

Abstract

The effect of a chronic exposure to sublethal concentration of mercuric chloride (0.3 mg/1) on the activities of some enzymes in the digestive system of the teleost fish Channa punctatus was examined after 15 and 30 days of treatment. Glucose‐6‐phosphatase was significantly inhibited in the intestine and pyloric caeca. No marked alterations were observed in the activities of maltase and lactase except for elevation in maltase activity and inhibition in lactase activity in the intestine and pyloric caeca after 15 days of treatment. Three peptidases (aminotripeptidase, glycylglycine dipeptidase and glycyl‐1‐leucine dipeptidase) showed decreased activities in all parts of the digestive system. A decrease was also observed in the activity of lipase except for the stomach where inhibition after 15 days was insignificant. The results indicate that the activities of all the enzymes examined are inhibited in intestine and pyloric caeca and digestion of proteins and lipids may be more affected by mercury than the digestion of some carbohydrates.     

Bioaccumulation studies of organochlorinated pesticides in tissues of Cyprinus carpio

Freshwater fish Cyprinus carpio was selected for the study of bioaccumulation of organochlorinated pesticides in tissues like gills, muscle, intestine, kidney, and liver in a continuous fed system. The pesticides used were Aldrin, Dieldrin, BHC, and DDT. The bioaccumulation of Dieldrin was maximum of 85.0 microg g(-1) wet weight in liver tissue while minimum of 7.30 microg g(-1) wet weight for DDT at 30 days exposure time. Bioconcentration factor (BCF) has followed the same trend in liver tissue for Dieldrin and DDT. The rate of bioaccumulation was found to be maximum of 4.3879 microg g(-1) wet weight in liver tissue and minimum of 0.0021 microg g(-1) wet weight in gill tissue for 30 days exposure. As evidenced by the increasing values of BCF, pesticide uptake also showed increased trend with the increase in exposure time. A high correlation coefficient ranging between 0.7247 and 0.9616 between the pesticide concentration and exposure time was observed. Based on actual BCF values, log Kow were calculated and the values are well within the reported values of 6.5 indicating efficient relationship between BCF and log Kow because beyond the 6.5 the bioconcentration levels off.     

The effects of ethylene chlorohydrin on fatty acid synthesis

Male chicks weighing 700 to 900 g. received an acute or eight doses IG of 60 or 40 mg/kg ethylene chlorohydrin (ECH) respectively and were sacrificed eighteen hours after the last dose. Mitochondrial elongation of fatty acids was decreased significantly while fatty acid synthetase activity was not significantly affected by ECH treatment. Cytochrome c oxidase activity in fresh whole liver homogenate was significantly higher in chicks subjected to acute exposure with ECH when compared to the controls. Upon freezing and thawing of homogenates, cytochrome c oxidase activity increased significantly in the control group but was unchanged in the ECH group which suggests that the mitochondrial membrane integrity is compromised by the ECH treatment. Serum and liver triglyceride levels were significantly elevated in both the single and multiple ECH dose groups. Liver to body weight ratios were significantly higher in both treatment groups when compared to their controls. Histological examination of the liver of ECH-treated chicks showed cytoplasmic clearing of the cells but no vacuolization or centrilobular necrosis. Serum isocitrate dehydrogenase levels were significantly higher in the multiple treatment ECH group than in the control group.     

Induction of rat hepatic microsomal enzymes by toxaphene pretreatment

Abstract

The effects of pretreatment of rats with toxaphene on hepatic drug metabolizing enzymes and several other parameters of the mixed function oxidase system were investigated. Adult male Sprague‐Dawley rats were fed diets containing 0, 50, 100, 150 and 200 ppm of toxaphene for 14 days. The body weight gain was unaltered as well as the food consumption in all the toxaphene fed groups. There was no change in the weights of brain, kidney, heart, and testes but the liver weight was significantly increased. The thymus weight in all the toxaphene fed groups was decreased. Hydroxylation of pentobarbital and aniline was significantly enhanced in rats exposed to toxaphene. Ethylmorphine‐N‐demethy‐lase activity in the toxaphene treated rats was also elevated. Enhanced hydroxylation of pentobarbital was also evident from the decreased sleeping time following pentobarbital administration. Exposure to toxaphene increased cytochrome P‐450, NADPH‐cytochrome c‐reductase and dehydrogenase in hepatic microsomal fractions. The binding of aniline and hexobarbital to microsomes was also enhanced, suggesting that the intermediate steps in the electron‐transfer system were increased. In conclusion, pretreatment of rats with toxaphene for fourteen days resulted in the induction of the hepatic mixed function oxidase system.     

The effects of ethylene chlorohydrin on fatty acid synthesis 1 2 3

Abstract

Male chicks weighing 700 to 900 g. received an acute or eight doses IG of 60 or 40 mg/kg ethylene chlorohydrin (ECH) respectively and were sacrificed eighteen hours after the last dose. Mitochondrial elongation of fatty acids was decreased significantly while fatty acid synthetase activity was not significantly affected by ECH treatment. Cytochrome c oxidase activity in fresh whole liver homogenate was significantly higher in chicks subjected to acute exposure with ECH when compared to the controls. Upon freezing and thawing of homogenates, cytochrome c oxidase activity increased significantly in the control group but was unchanged in the ECH group which suggests that the mitochondrial membrane integrity is compromised by the ECH treatment. Serum and liver triglyceride levels were significantly elevated in both the single and multiple ECH dose groups. Liver to body weight ratios were significantly higher in both treatment groups when compared to their controls. Histological examination of the liver of ECH‐treated chicks showed cytoplasmic clearing of the cells but no vacuolization or centri‐lobular necrosis. Serum isocitrate dehydrogenase levels were significantly higher in the multiple treatment ECH group than in the control group.     

Mercury induced time-dependent alterations in lipid profiles and lipid peroxidation in different body organs of cat-fish Heteropneustes fossilis

The effects of mercuric chloride (HgCl2) on lipid profiles and lipid peroxidation in different body organs of fresh water cat-fish Heteropneustes fossilis were studied. The daily exposure of HgCl2 0.2 mg/L for 10, 20 and 30 days depleted the total lipids in brain. But the content of phospholipids enhanced significantly at 30 days. Significant diminution in C/P ratio was discernible with 30 days of exposure following mercury toxicosis. Liver exhibited elevated levels of total lipids, phospholipids, cholesterol and C/P ratio. Interestingly kidney showed marked decrease in the concentration of total lipids, cholesterol and C/P ratio at higher exposure. However, the phospholipid values increased during the longer exposure. The content of total lipids and phospholipids was high in muscle but the level of cholesterol and C/P ratio were depleted. Significant increment in lipid peroxidation was discernible in brain, liver and muscle. In kidney the rate of lipid peroxidation was significantly reduced. The results suggest that exposure of HgCl2 enhances the peroxidation of endogenous lipids in brain, liver and muscle. Interestingly the lipid contents are affected differently in different body organs.