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.     

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.     

Diazinon treatment effects on heart and skeletal muscle enzyme activities

Abstract

The effects of low levels of diazinon treatment on four marker enzymes in rat heart and skeletal muscle have been investigated. Adult male Wistar rats were treated twice a week with a dose of 0.5 ml‐kg^‐1day^‐1 diazinon for 28 weeks. Diazinon treated rats gained significantly less weight than Sham‐treated controls. Typical differences in Succinate dehydrogenase (SDH), Lactate dehydrogenase (LDH), Phosphofructo kinase (PFK) and Hexokinase (HK) activities were observed between heart and skeletal muscles. Diazinon feeding had no effect on heart, soleus, gastrocnemius and plantaris SDH, LDH and PFK enzyme activities after 28 weeks. HK activity was significantly increased in sham‐control soieus and plantaris muscles after 28 weeks. Diazinon feeding inhibited HK activity in plantaris muscle after 28 weeks treatment These results demonstrate that chronic low levels of diazinon have little effect on the glycolytic and oxidative activity in heart and skeletal muscle.     

Subacute effects of a phosphorothionate pesticide on mixed function oxidases of wistar rats

Abstract

Subacute oral toxicity of a newly developed phosphorothionate insecticide (2‐butenoic acid‐3‐(diethoxy‐phosphinothioyl) methyl ester), coded as RPR‐2, was studied in male rats by oral (multiple) intubation of low (0.014 mg kg^‐1 day^‐1), medium (0.028 mg kg^‐1 day^‐1), and high (0.042 mg kg^‐1 day^‐1) dose for 90 days. The medium and high dose produced toxic symptoms along‐with some mortality (20%) occurred in the high dose treated rats. The medium and high doses caused significant inhibition in cytochrome P‐450 activity in liver, lung, kidney and brain tissues at 45 and 90 days. The high dose caused significant decrease in cyt.b₅ activity of all the four tissues at 45 and 90 days. Whereas, medium dose brought such effect in liver and lung at 45 and 90 days. Kidney and brain cyt.b₅ activity decreased significantly at 90^th day due to medium dose. Low dose also caused inhibition in cyt.b₅ activity in brain at 90^th day. Cytochrome P‐450 reductase activity was decreased significantly in liver, lung, kidney and brain at 45 and 90^th by the medium and high dose. The results indicated that RPR‐2 had potential to modulate hepatic and extra‐hepatic cyt.P‐450 dependent monooxygenase system of rat due to subacute exposure. These metabolic alterations were quite reversible after 28 days withdrawal of treatment.     

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

Alterations in the activities of some enzymes in the brain, gills, intestine, kidney, liver and muscles have been examined in the fresh water murrel, , 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.     

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.     

In vivo chronic effect of dimethoate and deltamethrin on rabbits

The in vivo effect of dimethoate and deltamethrin on body and organ weights, serum proteins and on plasma acetylcholinesterase (AChE), aromatic esterase and ATPase were examined in growing male rabbits throughout five months period. Both compounds had no significant effect on body weight; however, adrenal, testis & pituitary weights decreased (P less than 0.01); the liver and spleen weights increased (P less than 0.01) in a dose dependent manner. Serum total proteins and globulin decreased (P less than 0.01) in a dose dependent trend, while serum albumin was not greatly affected. AChE activity was increased (P less than 0.01) after 1 month of treatment with the two doses of dimethoate and deltamethrin; thereafter, AChE activity showed 40% inhibition of the control level. The activity of aromatic esterase increased markedly after the first month, then declined gradually until the fifth month. High dose of dimethoate markedly inhibited this enzyme particularly after the 5th month of treatment. Both doses of deltamethrin increased ATPase activity after the first month of treatment, then the ATPase activity was normal. Dimethoate inhibited ATPase particularly at the end of treatment in a dose dependent manner.     

Toxicity of pirimiphos-methyl: I. The acute and subacute oral toxicity in albino rats

In an acute study, albino rats of both sexes were orally administered graded doses of Pirimiphosmethyl, and the statistically computed median lethal dose (LD-50) were 1861 and 1667 mg/kg body weight for male and female rats respectively. No treatment related changes were discernible with regard to food intake, growth, gross or histopathology of the organs. In a time-course study, the correlation between symptoms and degree of esterase inhibition was examined in rats administered the minimum lethal dose (MLD: 1000 mg/kg b.w.) of the insecticide. Time-course inhibition pattern of both cholinesterase (ChE) and non-specific carboxylesterase (NSE) activities in brain and plasma revealed maximum inhibition at 24 h post-treatment which correlated well with the intensity of symptoms. In a subacute study, groups of male rats were fed dietary Pirimiphos-methyl at 0, 10, 250, 500 and 1000 ppm for 28 days. Food consumption and growth rate were not affected throughout the experimental period. At necropsy after 28 days, no gross pathological changes were seen in any of the organs except a slight increase in liver weight at 1000 ppm. Though no statistical differences were observed in the levels of hepatic transaminases, a significant increase in serum transaminase was evident. Significant increase in the activities of hepatic ALP, beta-GLR and serum ALP were evident at 500 and 1000 ppm. Further, significant inhibition of plasma PChE was evident at 250, 500 and 1000 ppm while the degree of inhibition of brain AChE was significant only at the higher dosages. No histopathological alterations were observed in any of the organs.     

Bioavailability and biological activity of bound residues of radiolabelled pirimiphos-methyl in maize grains.

Using a 14C-labelled pirimiphos-methyl preparation, the percentage of pirimiphos-methyl residues bound to maize grains after 32 weeks of storage was 13% of the applied dosage, or 38% of total terminal residues. Evidence is presented to show that bound residues of pirimiphos-methyl are bioavailable to the rat: 30%, 2% and approx. 6% of radioactivity were measured in urine expired air, and some organs respectively. A major portion of radioactivity (55%) was eliminated through faeces. Grain-bound pirimiphos-methyl residues (generated after storing whole maize grains with pirimiphos-methyl at concentrations of 10 ppm and 100 ppm) were administered to albino rats for 12 weeks. Body and organ weights, enzyme activities and blood chemistry were tested. There was a significant reduction in body weight gain in female rats. Also a significant reduction in blood cholinesterase activity was observed in both male and female rats fed on grain bound pirimiphos-methyl residues at two dose levels. The white blood cell count increased significantly in male rats fed on the high dose. No significant changes were observed in the other blood chemistry parameters tested. The results indicate that maize-bound pirimiphos-methyl residues can exert adverse biological effects in the rat.     

Antioxidant effect of Sargassum polycystum (Phaeophyceae) against acetaminophen induced changes in hepatic mitochondrial enzymes during toxic hepatitis

The present study was aimed to examine the protective effects of Sargassum polycystum (Phaeophyceae) alcoholic extract on changes in liver mitochondrial enzymes against acetaminophen induced toxic hepatitis in experimental rats. The levels of protein, lipid peroxide, glutathione (GSH) in mitochondrial fraction, superoxide dismutase (SOD) and catalase (CAT) were also determined. The activities of tricarboxylic acid enzymes such as isocitrate dehydrogenase (ICD), alpha-ketoglutarate dehydrogenase (alpha-KGD), succinate dehydrogenase (SD), malate dehydrogenase (MD), NADH dehydrogenase, and cytochrome-c-oxidase were determined in mitochondrial fraction. The rats intoxicated with acetaminophen showed significant elevation in the levels of lipid peroxides with decreased levels of protein, GSH, SOD, CAT and impaired tricarboxylic acid cycle enzyme activities. The prior oral administration of S. polycystum alcoholic extract showed significant diminution in the severity of toxic hepatitis in acetaminophen-induced rats by maintaining the activities of tricarboxylic acid enzymes with concomitant improvement in the hepatic mitochondrial antiperoxidative status when compared with intoxicated animals. The results obtained in the present study indicate that the protective effects of S. polycystum extract may be due to the presence of some active compounds that are inhibitory against the free radicals generated during lipid peroxidation in acetaminophen induced toxic hepatitis.     

Subacute effects of a phosphorothionate pesticide on mixed function oxidases of Wistar rats

Subacute oral toxicity of a newly developed phosphorothionate insecticide (2-butenoic acid-3-(diethoxy-phosphinothioyl) methyl ester), coded as RPR-2, was studied in male rats by oral (multiple) intubation of low (0.014 mg kg(-1) day(-1)), medium (0.028 mg kg(-1) day(-1)), and high (0.042 mg kg(-1) day(-1)) dose for 90 days. The medium and high dose produced toxic symptoms along-with some mortality (20%) occurred in the high dose treated rats. The medium and high doses caused significant inhibition in cytochrome P-450 activity in liver, lung, kidney and brain tissues at 45 and 90 days. The high dose caused significant decrease in cyt.b5 activity of all the four tissues at 45 and 90 days. Whereas, medium dose brought such effect in liver and lung at 45 and 90 days. Kidney and brain cyt.b5 activity decreased significantly at 90th day due to medium dose. Low dose also caused inhibition in cyt.b5 activity in brain at 90th day. Cytochrome P-450 reductase activity was decreased significantly in liver,     

Study on 14C-BHA absorption and distribution in rat

BHA was administered to rats at doses of 5 or 500 mg/kg for seven days. ¹⁴C-BHA absorption was investigated on the eighth day and compared with animals receiving a single dose of 5 or 500 mg/kg BHA. Absorption of ¹⁴C-BHA was proportionately greater at the high dose rats. ¹⁴C distribution was 3–6 times higher in the forestomach than in the pyloric region of the stomach. The urinary excretion of BHA conjugates was not dependent on pretreatment with BHA or on the dose.     

Occupational effect of phosfolan insecticide on spraymen during field exposure.

Phosfolan (Cyolane), 2-(diethoxy phosphinylimino)-1,3-dithiolane is one of the widely used insecticides in Egypt specially to protect cotton plants. The hazard of exposure of the spray workers team in the field was estimated in terms of the amount of Phosfolan insecticide retained on workmen body pads during field spraying. The health effect of such exposure was determined through recording of the AChE inhibition in the red blood cells at different intervals after exposure. The calculated percentage of the toxic dose received per every spraying day for each worker varied with the type of job in the range of 0.008 to 0.03 percent. The body of the mixer received the maximum exposure with 10 to 12 fold that of the assistants. The highly exposed group of workers suffered from 31 to 44 percent RBC's AChE inhibition. About half of the inhibited enzyme activity recovered after 48 hours. Then it took more than 3-4 weeks to reach complete recovery. Thus the RBC's AChE activity can be recommended as a criterion for the level of exposure to organophosphorous insecticides.     

Lipid peroxidation and antioxidant enzyme activity in different organs of mice exposed to low level of mercury

The effects of mercuric chloride (Hg) on lipid peroxidation (LPO), glutathione reductase (GR), glutathione peroxidase (GPx), superoxide dismutase (SOD) and glutathione (GSH) levels in different organs of mice (CD-1) were evaluated. Mice were exposed (2 days/week) to 0.0 (control), 0.8 (low) and 8.0 (mid) and 80.0 (high) gHg/kg/day for 2 weeks. The high dose group was excluded from the study due to high mortality. LPO levels in kidney, testis and epididymus at low and mid doses; GR and GPx levels in testis at mid dose; SOD levels in brain and testis at both doses, liver and epididymus at mid dose; GSH levels in testis at both doses were significantly increased compared to their controls. However, the GR levels in kidney at both doses and in epididymus at mid dose; GPx levels in kidney and epididymus and SOD levels in kidney at both the doses; GSH levels in epididymus at mid dose were significantly decreased compared to their control. Body weight gain and food efficiency were significantly reduced (p<0.05) in mid dose. These results indicated that Hg treatment enhanced LPO in all tissues, but showed significant enhancement only in kidney, testis and epididymus suggesting that these organs were more susceptible to Hg toxicity. The increase in antioxidant enzyme levels in testis could be a mechanism protecting the cells against reactive oxygen species.     

EFFECTS OF SELENIUM AND MERCURY ON THE ENZYMATIC ACTIVITIES AND LIPID PEROXIDATION IN BRAIN,LIVER, AND BLOOD OF RATS

Recent studies have reported on the toxicity and related oxidative stress of selenium and mercury. The present study compares the effects of Se as sodium selenite (Na₂SeO₃) and Hg as mercuric chloride (HgCl₂) separately and in combination. Rats received repeated oral doses of Se (0.5 μmol/ml), Hg (0.5 μmol/ml), or Se in combination with Hg (0.5 μmol/ml of each) for 5 consecutive days. Rat serum, brain and liver samples were collected for biochemical assays. The following biochemical alterations occurred in response to Hg treatment: protein content (brain and liver), acetylcholinesterase (AChE) (brain and serum), acid and alkaline (AcP and AlP) phosphatases (plasma and liver) and glutathione S-transferase (GST) (plasma and liver) activities were significantly (P<0.05) decreased, while lactate dehydrogenase (LDH) (plasma, brain and liver), aspartate and alanine aminotransferase (AST, ALT) (serum and liver) activities were significantly increased. Thiobarbituric acid reactive substances (TBARS) was significantly increased in brain and liver. Effect of Se alone included decreased AcP, AlP and GST (serum and liver) activities. However, LDH (serum, brain and liver) and AST (liver) and TBARS (brain and liver) increased. Selenium in combination with Hg partially or totally alleviated the toxic effects of Hg on different studied enzymes. It is concluded that Se could be able to antagonize the toxic effects of mercury.     

Bioavailability and toxicological potential of lentil-bound residues of malathion in rats.

Lentil grains treated with malathion and stored under laboratory conditions for 12 months formed bound residues. Bioavailability and the effects of lentil-bound residues of malathion in rats were studied. The amount of bound residues in lentils treated with 14C-malathion at 10 ppm and 50 ppm gradually increased to 9.52% and 13.01% of the initially applied doses after 12 months. When rats were fed these 14C-bound residues, radioactivity excreted in urine accounted for 34.49% of the administered dose. In feces, 26.15% of given dose was methanol-extractable while 18.67% was determined as nonextractable. Various tissues including liver, kidney, fat and lungs contained 8.93% while radioactivity in expired air (14CO2) was low (1.51%). The results indicate that lentil-bound malathion residues are highly bioavailable to rats. Analysis of the lentil material containing bound residues indicated that the main compound was malathion. Lentil-bound malathion residues were administered to albino rats at 0.95 and 6.51 ppm in the feed for 3 months. Body weights were determined during and at the end of the experiment. Terminal organ weights were also determined and a number of blood chemistry parameters were examined. A significant reduction in serum cholinesterase activity and an increase in blood urea nitrogen and in white cell count suggest a toxocological potential of the bound residues.     

Effect of cadmium on ATPase activities in rats fed on iron-deficient and sufficient diets

Male Sprague-Dawley rats were fed on different levels of cadmium mixed with purified diets containing iron or no iron for 8 weeks. The body weight gain, tissue weights, hemoglobin, hematocrit, liver and brain ATPase were measured at 2, 4 and 8 weeks after feeding. The hemoglobin and hematocrit values were the same in all rats fed on cadmium. The rats fed on iron-deficient diets mixed with cadmium showed a significant decrease in body weight gain. However, the rats receiving only the 100 ppm of cadmium in iron-sufficient diet showed a significant decrease in body weight gain. There were no significant changes in the weights of thymus, spleen, kidney, heart, brain and testes. However, the liver weights were decreased in the highest treatment of cadmium but the liver weight/body ratios were uneffected. Na+-K+ activated ATPase activity in brains of rats fed on cadmium were significantly decreased at 2, 4 and 8 weeks of treatment. The decrease was more pronounced in rats fed on iron-deficient diets. Oligomycin-sensitive (Mitochondrial) Mg2+ ATPase activity was also significantly decreased in liver and brain tissues of rats fed on cadmium. Oligomycin-insensitive Mg2+ ATPase activity, however, was not altered in any tissues tested. It appears that cadmium may be interfering with energy (ATP) production and utilization processes in rat brain and liver tissues.     

Photomirex: A teratogenicity and tissue distribution study in the rabbit

Abstract

Adult New Zealand white does were intubated orally with single daily doses of 0, 5, or 10 mg of photomirex (8‐monohydromirex) per kg body weight from the 6th through to the 18th day of gestation. Pregnancies were interrupted at term by cesarian section and fetuses removed and evaluated by following routine teratologic methods. Both maternal and fetal tissues were analyzed for residues of photomirex. None of the treated does showed any sign of toxicity. Except for a significant reduction in the mean fetal weight of the 10 mg/kg group all other parameters which evaluated fetal survival and fetal development were within the control range. Photomirex was found in all tissues examined. In the doe, the highest levels were found in fat followed by liver, kidney, spleen, heart, brain and blood. Photomirex was readily transferred across the placenta and accumulated in the fetus. However, in the fetus the highest levels were found in the heart, followed by liver, brain and blood. There were no teratogenic effects at the doses used in this study.     

LIPID PEROXIDATION AND ANTIOXIDANT ENZYME ACTIVITY IN DIFFERENT ORGANS OF MICE EXPOSED TO LOW LEVEL OF MERCURY

The effects of mercuric chloride (Hg) on lipid peroxidation (LPO), glutathione reductase (GR), glutathione peroxidase (GPx), superoxide dismutase (SOD) and glutathione (GSH) levels in different organs of mice (CD-1) were evaluated. Mice were exposed (2 days/week) to 0.0 (control), 0.8 (low) and 8.0 (mid) and 80.0 (high) gHg/kg/day for 2 weeks. The high dose group was excluded from the study due to high mortality. LPO levels in kidney, testis and epididymus at low and mid doses; GR and GPx levels in testis at mid dose; SOD levels in brain and testis at both doses, liver and epididymus at mid dose; GSH levels in testis at both doses were significantly increased compared to their controls. However, the GR levels in kidney at both doses and in epididymus at mid dose; GPx levels in kidney and epididymus and SOD levels in kidney at both the doses; GSH levels in epididymus at mid dose were significantly decreased compared to their control. Body weight gain and food efficiency were significantly reduced (<0.05) in mid dose. These results indicated that Hg treatment enhanced LPO in all tissues, but showed significant enhancement only in kidney, testis and epididymus suggesting that these organs were more susceptible to Hg toxicity. The increase in antioxidant enzyme levels in testis could be a mechanism protecting the cells against reactive oxygen species.     

Impact of the toxicity of Cylindrospermopsis raciborskii (Woloszynska) Seenayya & Subba Raju on laboratory rats in vivo

In vivo laboratory studies of toxicity were performed on Wistar rats using a methanol extract produced by the natural population of Cylindrospermopsis raciborskii (abundance of 2.13 × 10⁵ trichomes mL⁻¹) collected at Aleksandrovac Lake (Serbia). HPLC analysis showed that the extract contains 6.65 μg cylindrospermopsin (CYN) mg⁻¹. The rats were killed 24 or 72 h after a single intraperitoneal injection of C. raciborskii extract in concentrations of 1500, 3000, 6000 and 12,000 μg kg⁻¹ body weight (bw) and an equivalent amount of CYN as present in the highest dose of the extract (79.80 μg CYN kg⁻¹ bw). The genotoxic effect on the livers treated with C. raciborskii was evaluated using comet assay and potential induction of oxidative stress as the toxicity mechanism associated with the presence of CYN in extract. The results from the analyses of DNA damage in the comet tail length, tail moment and percentage of DNA in the tail in the liver indicated that administration of extract and CYN present statistically significant difference when compared with the negative control group. Although an increase in the frequency of selected parameters induced by the CYN was observed in the liver, this damage was less than the damage resulting from the administration of the highest dose of extract. The changes in the biochemical parameters of the hepatic damage showed that the application of single doses of the extract and CYN did not cause serious liver damage in rats. The extract and CYN significantly increased oxidative stress in rats’ liver after a single exposure.