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Biomedical subjects

M K Krishnakumari

Publications and source records attributed to M K Krishnakumari.

At least 19 recordsLinked to original sources
PubMed1995

Prenatal toxicity of heptachlor in albino rats.

Exposure of the cyclodiene insecticide heptachlor at 1/8 and 1/4 LD50 to male and female albino rats before mating affected fertility in both sexes. A decrease in implantations, serum oestrogen and progesterone levels and increase in resorptions in the females was observed. However, no histological changes were observed except for few atretic follicles in the treated females. In males, a dose-dependent significant decrease in the sperm count and coagulating gland fructose levels was observed, with marginal degeneration of seminiferous tubules. These results are indicative of the prenatal toxicity of heptachlor in male and female rats.

Animals↗
PubMed1992

Effect of vitamin A on hexachlorocyclohexane (HCH) toxicity in the rat.

1. Technical hexachlorocyclohexane (HCH) depleted hepatic stores of vitamin A in male albino rats to cause secondary vitamin A deficiency. 2. Toxicity of HCH in rats is augmented by dietary vitamin A-deficiency as evidenced by growth retardation, organ hypertrophies and alterations in the serum and liver levels of the marker enzymes of toxicity. 3. Supplementation of dietary vitamin A to the rats either in adequate (2000 IU/kg diet) or in an excess but not hypervitaminotic level (10(5) IU/kg diet) resulted in significant protection against the toxicity of HCH. 4. The activities of the hepatic xenobiotic metabolizing enzymes were generally low (with the exception of glutathione S-transferase) in the vitamin A-deficient rats compared to those of the vitamin A supplemented diet groups. 5. The results indicated that dietary vitamin A influences the response of male albino rats to HCH toxicity possibly by modulating the activities of hepatic xenobiotic metabolizing enzymes.

Animals↗
PubMed1992

Role of vitamin A in the haematotoxicity of hexachlorocyclohexane (HCH) in the rat.

The haematotoxicity of technical hexachlorocyclohexane (HCH) (1000 ppm) was investigated in male albino rats fed with diet free of vitamin A or containing vitamin A at 2000 or 10(5) I.U./kg. Assessment of HCH-induced haematotoxicity at the end of the 7 weeks feeding period was done on the basis of haemoglobin content, total count of red blood cells and white blood cells and the differential counts of the white blood cells as well as by parameters such as packed cell volume, mean corpuscular volume, mean corpuscular haemoglobin, mean corpuscular haemoglobin content, prothrombin time and clotting time. In the rats fed with vitamin A-free diet containing HCH, significant reductions were noticed in the total white blood cells count, clotting time and prothrombin time indicating severe haematotoxicity. Differential count of the white blood cells of these rats revealed a non-significant reduction in the lymphocyte count. The only indication of haematotoxicity caused by hexachlorocyclohexane in the vitamin A supplemented rats was a slight but statistically significant reduction of the total count of white blood cells. These results demonstrate that the haematotoxicity of hexachlorocyclohexane in the rats is enhanced by vitamin A-deficiency and its supplementation particularly in excess but not at hypervitaminotic level is protective against the toxicity.

Animals↗
PubMed1990

Protective role of vitamin A in the male reproductive toxicity of hexachlorocyclohexane (HCH) in the rat.

The reproductive toxicity of the organochlorine insecticide, hexachlorocyclohexane (HCH), was investigated in male albino rats fed a diet free of vitamin A or containing vitamin A at 2000 or 100,000 IU/kg diet. Diets containing 1000 ppm HCH for 7 weeks did not cause testicular toxicity in the vitamin-A-deficient and supplemented rats. However, reproductive toxicity was clearly manifested 2 weeks after withdrawing HCH from the diets and was more pronounced in the vitamin A deficient rats compared to their vitamin A supplemented counterparts. Reduction in the testicular weights was accompanied by atrophy of epididymides and seminal vesicles in the vitamin A deficient rats alone. Inhibition of spermatogenesis was further confirmed by decreased sperm count in the epididymis. Biochemically, the activities of the steroidogenic enzymes were drastically reduced. Supplementation of vitamin A after withdrawal of HCH accelerated the recovery and restored spermatogenesis and enzyme activities in the deficient rats. These results demonstrate the greater susceptibility of the male reproductive system to HCH toxicity during vitamin A deficiency and also the protective effect of vitamin A supplementation.

Animals↗
PubMed1989

Inhibitory pattern of tissue esterases in rats fed dietary pirimiphos-methyl.

Activities of Acetylcholinesterase (AChE) in brain and erythrocytes, pseudocholinesterase (PChE) in plasma and non-specific carboxylesterase (NSE) in brain, liver, plasma and kidney were assayed at weekly intervals in growing male rats fed dietary pirimiphos-methyl at dosages of 1000, and 1500 ppm for a period of 28 days. Significant inhibition of tissue esterases were observed at the end of 7 days at both the dosages and the enzyme activities remained markedly inhibited at subsequent intervals. Activities of all enzymes (excepting Brain AChE) returned to normal levels following a 7-day maintenance on the insecticide-free diet implicating that pirimiphos-methyl induced little or no permanent tissue damage. The results suggest that plasma NSE level may also serve as a sensitive indicator in monitoring OPI exposure.

Animals↗
PubMed1989

Cytotoxicity of certain organic solvents and organophosphorus insecticides to the ciliated protozoan Paramecium caudatum.

Responses of Paramecium caudatum, a ciliated protozoan, to acute exposures of certain organic solvents and organophosphorus insecticides (OPI) were studied by determining their lethal concentration (10 min-LC100) and median lethal concentration (4 h-LC50). The solvents and OPI evoked a distinct sequence of responses. Among the five solvents tested, acetone proved most toxic [LC-2.9% and LC50-0.68% (v/v)], while dimethyl sulphoxide (DMSO) showed least toxicity [LC-11.0% and LC50-3.16% (v/v)]. The order of toxicity of solvents was: acetone greater than ethanol greater than methanol greater than N, N-dimethylformamide greater than dimethylsulphoxide. The LC values of six OPI dissolved in either acetone or DMSO indicated that they were more toxic when dissolved in acetone and least toxic in DMSO. Among the OPI, bromophos proved most toxic (LC-10 ppm) while malathion showed least toxicity (LC-200 ppm) in DMSO. The order of toxicity of OPI was: bromophos greater than pirimiphos-methyl greater than parathion methyl greater than dichlorvos greater than fenitrothion greater than malathion. The 4 h-LC50 values computed for bromophos and malathion (dissolved in DMSO) were 575 ppb and 19.9 ppm, respectively, indicating the high susceptibility of P. caudatum to bromophos. The results indicate that the Paramecium toxicity assay could be used as a complementary system to rapidly elucidate the cytotoxic potential of compounds.

Animals↗
PubMed1988

Response of blood and brain cholinesterase to dermal exposure of bromophos in the rat.

Response of cholinesterase to dermal exposure of acute, single and multiple doses of Bromophos in the female rat has been studied. Dose-response studies (50-4000 mg/kg body weight, 24 h exposure) showed that plasma cholinesterase was most sensitive to inhibition in vivo, followed by the brain and erythrocyte acetylcholinesterase. The ID50 values for the in vivo cholinesterase inhibition were 10.1, 576.1 and 1938.0 mg/kg body weight for the plasma, brain and erythrocytes, respectively. In time-course studies after a single sublethal dose of 1000 mg/kg body weight (24 h) of Bromophos, the serum and brain cholinesterase were rapidly inhibited reaching a maximum at 16 h. Recovery was complete in the case of serum at 14 days post-exposure, whereas the brain enzyme was not fully recovered at 21 days. In a subacute study, daily dermal application of 50 mg/kg body weight of Bromophos for 5 and 10 days, resulted in high inhibition of the serum cholinesterase and brain acetylcholinesterase, the former being more marked which was reversible after 10 or 15 days of post-exposure period. Very low levels of dermal exposure of Bromophos (10-50 mg/kg body weight) for 17 days caused pronounced depression of serum cholinesterase which completely recovered in 15 days after cessation of exposure suggesting that the serum cholinesterase could serve as the most sensitive diagnostic indicator of Bromophos exposure.

Animals↗
PubMed1988

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.

Animals↗
PubMed1988

Toxicity of pirimiphos-methyl: II. Effect of dietary feeding on blood and urine constituents in albino rats.

Growing male rats were fed dietary Pirimiphos-methyl at 0, 500, 1000 and 1500 ppm for 28 days and selected blood and urine constituents were measured at weekly intervals. Dietary intake of Pirimiphos-methyl induced an initial, transient hypoglycemia and a marked elevation in blood urea at all dosages. Though it did not produce any significant change in the urine output initially, marked oliguria was observed after 12 days of feeding. The alterations observed in urine constituents were: increased urea, proteinuria, transient increase in creatinine and significant increase in the excretion of glucuronic acid and ethereal sulfate at all intervals. However, since no pathological alterations were evident in the kidney, the anomalous urinary excretion of various body constituents might be due to the anticholinesterase action of the insecticide at the central nervous system.

Animals↗
PubMed1985

Effect of L-ascorbic acid supplementation on the toxicity of pirimiphos-methyl to albino rats.

The effect of L-ascorbic acid supplementation on Pirimiphos-methyl induced toxicity was studied in albino rats. Biochemical estimations were made in rats administered orally the insecticide at 100 and 200 mg/kg body weight with or without oral supplementation of L-ascorbic acid at 200 mg/kg b.w. The biochemical assessments included estimations of brain and plasma cholinesterases, levels of ascorbic acid in liver, kidney and adrenals, urinary levels of ascorbic acid and glucuronic acid. A lower degree of inhibition of the cholinesterases were evident in ascorbic acid supplemented rats. Marked elevation in urinary levels of ascorbic acid and glucuronic acid was observed in the insecticide treated rats. Results of this study suggests that L-ascorbic acid supplementation partially offsets Pirimiphos-methyl induced toxicity.

Acetylcholinesterase↗
PubMed1983

Toxicity of technical X-factor to weanling rats. II. A subacute oral study.

Eighty male weanling rats were fed dietary levels of Technical X-factor (beta-isomer free BHC, a by-product obtained during the separation of lindane from Tech. BHC) at dosages of 10,50,250,750,1500 and 3000 ppm for 90 days. No overt signs of toxicity or mortality were observed at any of the dietary levels. However, a significant reduction in food consumption and growth was evident beyond 750 ppm. Pronounced hepatomegaly observed at 1500 and 3000 ppm was associated with histological alterations such as cellular hypertrophy, cytoplasmic vacuolisation and focal necrosis. Adrenals showed cortical hypertrophy and highly vacuolated cytoplasm. Though a significant increase in the levels of SGOT was noted at 3000 ppm dosage, no appreciable changes were observed in the levels of SGPT and SLDH. Technical X-factor appeared to possess low chronic toxicity compared to Tech. BHC as evidenced by the various parameters studied. The observed low chronic toxicity of X-factor is probably due to the absence if beta-isomer and altered composition of delta and alpha isomers.

Animals↗
PubMed1983

Hexachlorocyclohexane-induced testicular dysfunction in rats.

Weanling male albino rats were fed 100, 750 and 1500 p.p.m. of technical HCH for 90 days. There was marked testicular atrophy with reduced tubule size and spermatogenetic arrest at 1500 p.p.m. Histochemically, there was accumulation of cholesterol-positive lipids in the Sertoli cells and the Leydig cells of the atrophied testis and biochemical estimation revealed significant increase of total lipid and cholesterol contents. Activities of delta 5 3 beta hydroxysteroid dehydrogenase (delta 5 3 beta HSDH), 17 beta hydroxysteroid dehydrogenase (17 beta HSDH) and glucose-6-phosphate dehydrogenase (G-6-PDH) in the interstitial cells were markedly decreased suggesting steroidogenic inhibition in the Leydig cells of the atrophied testis due to HCH feeding.

Animals↗
PubMed1983

Testicular atrophy in Gallus domesticus fed acute doses of copper fungicides.

Acute oral toxicity of the copper fungicides, copper sulphate and copper oxychloride, were studied in male Gallus domesticus. The median lethal dose for copper sulphate and copper oxychloride determined were 693 and 1263 mg/kg body weight, respectively. Severe diarrhea and delayed mortality (3 to 6 days) was characteristic of copper oxychloride. Liver weights were nearly doubled in birds fed copper oxychloride and marked dose-dependent testicular atrophy was noticed in both copper sulphate and copper oxychloride fed birds. Mild to severe spermatogenetic arrest concomitant with testicular atrophy was observed. Histochemically, the interstitial (Leydig) cells and seminiferous tubules showed intense accumulation of cholesterol-positive lipids. The degree of lipophilia appeared to be directly proportional to the extent of spermatogenetic arrest, and these results are suggestive of steroidogenic inhibition in the Leydig cells of the atrophied testis.

Animals↗
PubMed1982

Mammalian toxicity of Technical X-factor I. An acute oral study.

Intragastric administration of acute doses of Technical X-factor (beta-isomer free BHC, a byproduct obtained during separation of Lindane from Tech. BHC) carried in peanut oil elicited typical signs of central nervous system depression in adult rats. The computed oral LD50 values of X-factor were 4174 and 5673 mg/kg. body weight for male and female rats respectively indicating that its acute toxicity was of relatively low order compared to Tech. BHC. It is suggested that the low acute mammalian toxicity of X-factor could possibly be due to a direct antagonism of the delta isomer (present in larger proportion in X-factor) with the gamma isomer.

Animals↗