PubMed Health⌕ Search

Biomedical subjects

K P Pandya

Publications and source records attributed to K P Pandya.

At least 19 recordsLinked to original sources

Modulation of benzene induced toxicity by protein A.

Administration of benzene (i.p. 1.0 mL/kg body weight) for 3 consecutive days produced leucopenia and lymphocytopenia in female albino rats. In addition, the total iron content, lipid peroxidation and superoxide dismutase activity of the liver and bone marrow were significantly (P < 0.001) increased. Low molecular weight (LMW) bleomycin-detectable iron accumulated only in bone marrow. Prior administration of Protein A (PA), a multipotent immunostimulant and interferon inducer (60 micrograms/kg body weight, i.v. twice weekly for 2 weeks), ameliorated most of the adverse effects of benzene. PA restored the changes in hepatic histological architecture, reversed leucopenia and superoxide dismutase activity, lipid peroxidation, total iron content and LMW iron content of bone marrow were normalized. Isozymes of glutathione-S-transferase (alpha, pi, mu) which decreased following benzene exposure increased in PA pretreated benzene exposed rats. This study suggests that pretreatment with PA modulates the toxicity of benzene.

Animals↗

Trichloroethylene toxicity in mice: a biochemical, hematological and pathological assessment.

Oral administration of trichloroethylene (TCE; 0, 500, 1000 and 2000 mg/kg/day) to male mice once daily, 5 days a week for a period of 28 days, caused a significant increase in liver weight, degeneration/necrosis of hepatocytes and characteristics proliferation of endothelial cells of hepatic sinusoids. Increase in kidney weight, glomerular nephrosis, degeneration/desquamation of tubular epithelium and characteristic amyloid deposition in glomeruli were observed only in the group of mice treated with 2000 mg/kg TCE. These changes occurred concurrently with a significant increase in total protein and free sulphydryl contents, elevated activities of acid phosphatase and catalase and decreased activity of delta-aminolevulinic acid dehydratase (delta-ALAD) indicating the sensitivity of liver and kidney as target tissues in TCE-toxicity. Hematological studies showed a significant increase in RBC counts and a reduction in WBC counts without any statistically significant change in the hemoglobin, urea nitrogen, creatinine and uric acid levels in the blood of TCE-exposed mice. A dose-related increase in cell density and acid phosphatase activity with a parallel significant decrease in the activity of delta-ALAD were observed in the bone marrow, which appear to be responsible for hematological alterations in TCE-exposed mice. The results suggest that early metabolic, pathological and hematological perturbations following a short-term exposure of TCE in mice, can provide the basis for its documented potential for chronic effects like blood dyscrasia and cancer.

Animals↗

An investigation of environmental impact on health of workers at retail petrol pumps.

Ninety-four male pump workers, employed in 41 petrol filling stations in Kanpur (formerly Cawnpore) and Lucknow--both in the Ganges plain of north India--were clinically examined. Headache, redness in eyes, lacrimation and signs like coated and/or furred tongue, throat and/or conjunctival congestion and carious teeth were significantly higher (P less than 0.05) in workers exposed to petrol fumes than in controls, as also was the level of phenol in urine (P less than 0.01). Environmental measurements revealed higher concentrations of benzene, sulphur dioxide and photoionizable dust in the air at petrol stations, and most of the symptoms and signs could be attributed to petrol fumes and other environmental pollution.

Adolescent↗

Induction of glutathione-S-transferase isoenzymes by protein A in rat liver.

The administration of Protein A, a cell wall protein of Staphylococcus aureus Cowan I cells, causes an induction of glutathione-s-transferase in rat liver. Proteins, cross reactive with anti human glutathione-s-transferase, acidic (pi), basic (alpha, and neutral (mu) isoenzymes, are induced by 5.8, 2.2 and 6.15 fold respectively. The induction of glutathione -s-transferases, at least in part, might play a role in manifestation of therapeutic properties of Protein A.

Animals↗

Accumulation of low molecular weight (bleomycin detectable) iron in bone marrow cells of rats after benzene exposure.

An accumulation of low molecular weight (LMW) bleomycin detectable iron in the bone marrow was observed after administration of benzene (IP 0.5 ml/kg, daily) for 5 and 10 days in female albino rats. However, this LMW iron was not detectable in the bone marrow of rats from the control group. Studies of bone marrow fractionation showed that the maximum accumulation of this LMW iron was in the mitochondrial fraction. An increase in the activity of superoxide dismutase and lipid peroxidation was also noticed in the benzene exposed groups.

Animals↗

Modulation of benzene toxicity by polyinosinic-polycytidilic acid, an interferon inducer.

Repeated intraperitoneal administration of benzene (1.0 ml/kg body wt.) for 3 days produced leucopenia, lymphocytopenia and significantly decreased body wt. (P less than 0.001) and organ weights of thymus (P less than 0.001) and spleen (P less than 0.001) in female albino rats. Total iron content, lipid peroxidation and superoxide dismutase activity of the liver and bone marrow were significantly increased as a result of benzene exposure. Low molecular weight (LMW) bleomycin detectable iron content was accumulated in bone marrow, whereas hepatic LMW iron was not detectable after benzene intoxication to rats. Prior administration of single dose (250 micrograms/100 g body wt.) of Poly IC, an interferon inducer with immunomodulating potential was found to be ameliorate some of the adverse effects of benzene as well as restoration of hepatic architecture histologically. Superoxide dismutase activity, lipid peroxidation, total iron content and LMW iron content (bone marrow) were normalised. Pretreatment of animals with Poly IC was able to enhance the SRBC antibody titre in benzene-treated animals. This study suggests that the beneficial effects of Poly IC in the amelioration of the acute toxicity of benzene has clinical significance.

Animals↗

Release of 2-thiobarbituric acid reactive products from glutamate or deoxyribonucleic acid by 1,2,4-benzenetriol or hydroquinone in the presence of copper ions.

Cytotoxic effects of various quinone compounds are thought to be due to the formation of semiquinone free radicals. Hydroquinone and 1,2,4-benzenetriol in the presence of copper ions release from glutamate or DNA aldehydic products capable of reacting with 2-thiobarbituric acid (TBA). The formation of TBA reactive products (TBAR) was greater in the presence of 1,2,4-benzenetriol in comparison with hydroquinone. Complete inhibition of formation of TBAR from glutamate by 1,2,4-benzenetriol and copper was observed in the presence of catalase, thiourea and mannitol. Albumin and superoxide dismutase offered substantial protection. Complete protection of formation of TBAR from DNA was observed in the presence of catalase and thiourea. Presence of albumin, mannitol and superoxide dismutase caused only partial inhibition. The formation of TBAR from glutamate or DNA is dependent on copper ion concentration. The present data indicate that hydroquinone and 1,2,4-benzenetriol in the presence of copper ions can lead to the formation of reactive hydroxyl radicals which can release TBAR from glutamate or DNA.

Albumins↗

Influence of trichloroethylene treatment on phosphoinositides in rat brain.

The effect of oral administration of trichloroethylene, a neurotoxic solvent, on the levels of phosphoinositides in rat brain was studied. Two hours after administration of a single dose of trichloroethylene (1000 mg/kg body wt.), the levels of phosphatidylinositol (PI) and phosphatidylinositol 4,5-biphosphate (PIP2) were reduced by 24 and 17%, respectively, without any significant change in that of phosphatidylinositol-4-phosphate (PIP). Twenty hours after treatment, the levels of PI and PIP2 were increased by 22 and 38%, respectively. Repeated administration of the same dose of trichloroethylene for 1 year markedly reduced the levels of PI (52%), PIP (23%) and PIP2 (45%). These results for the first time suggest the involvement of a phosphoinositide messenger system in trichloroethylene neurotoxicity.

Animals↗

Effect of hexacarbons on selected lipids in developing rat brain and peripheral nerves.

The effects of neurotoxic solvents, i.e. 2,5-hexanedione (2,5-HD), 2,5-hexanediol (2,5-HDiol) and the non-neurotoxic solvent, 2,4-hexanedione (2,4-HD) (500 mg/kg body wt./day, i.p.), have been studied on the lipid composition of brain and sciatic nerves in weanling rats. Five-day-old rats were administered a solvent daily for 21 days. Clinical signs of peripheral neuropathy appeared in 2,5-HD and 2,5-HDiol treated groups. Absolute weights of brain, spleen, thymus significantly decreased with 2,5-HD. Cholesterol content in whole brain homogenates and myelin was significantly reduced with 2,5-HD and 2,5-HDiol treatment. There was also a significant reduction in ubiquinone content of brain with 2,5-HD and 2,5-HDiol treatment. On exposure to neurotoxic chemicals to weanling rats, significant alteration in lipid profile was observed in the brain, which may be one of the key factors in the development of neuropathy.

Animals↗

Hepatotoxic effects elicited by n-hexane or n-heptane.

Hepatotoxic effects of n-hexane and n-heptane administered i.p. (1 ml/kg body wt) were studied in albino rats after 1, 2, 7 and 45 days of treatment. Hepatic protein content decreased with n-heptane and total sulphydryl content showed a significant decrease in the rats exposed to either solvent. A significant increase in lipid peroxidation was observed after 24 h and 48 h exposure to n-hexane or n-heptane. A marked decrease in drug metabolizing activity and an increase in pentabarbitone sleeping time was also observed. Hepatic glucose-6-phosphatase, a microsomal marker enzyme, showed a significant decrease.

Animals↗

Behavioral studies in petrol pump workers.

Behavioral studies were conducted on 90 petrol pump workers to study the effect of petrol on the central and peripheral nervous systems. Sixty-four control subjects of similar age and socio-economic status were also taken for purposes of comparison. Maudsley Personality Inventory (MPI), Benton Visual Retention Test, Digit Span Test, Progressive Matrices, Digit Symbol Test and Mirror Drawing Test were used for behavioral studies. Immediate and delayed memory were found to be significantly affected in exposed workers. Intellectual capacity and psychomotor ability were also significantly affected (P less than 0.01). Psychomotor ability and visuomotor learning ability were more affected (P less than 0.05) among the exposed subjects than among the controls. However, stability and extroversion-introversion ability remained unaffected.

Humans↗

Depletion of liver regulatory heme in benzene exposed rats.

The effect of a single dose of benzene (0.5 ml/kg body wt i.p.) on the heme saturation of tryptophan pyrrolase activity in liver was examined. There was a significant decrease in the heme saturation of hepatic tryptophan pyrrolase, suggesting depletion of "regulatory heme". After benzene administration there was significant increase in delta-aminolevulinate (ALA) synthetase activity (approx. 2-fold) while delta-aminolevulinate dehydratase activity was significantly decreased, however, ferrochelatase and heme oxygenase activities were unaltered. Administration of tryptophan to benzene pretreated rats showed a reversal of benzene effects on heme synthesizing enzymes: there is an increase in the heme saturation of tryptophan pyrrolase and decrease in delta-aminolevulinate synthetase. However, there was no significant alteration in the activity of delta-aminolevulinate dehydratase.

5-Aminolevulinate Synthetase↗

Relative toxicity of metabolites of benzene in mice.

Repeated ip administration of hydroquinone (10 mg/kg/day), benzoquinone (2 mg/kg/day) or benzenetriol (6.25 mg/kg/day) to rats for 6 weeks produced significant decreases in RBC and bone marrow cell counts and hemoglobin content, together with relative changes in organ weights. In addition, benzoquinone and benzenetriol elicited histological injuries in liver, thymus, spleen, kidney and peripheral lymph nodes which warrant further investigation.

Animals↗

Modulation of benzene toxicity by an interferon inducer (6MFA).

Repeated intraperitoneal administration of benzene (1.0 ml/kg body wt) for 3 days produced leucopenia, lymphocytopenia and an increased number of nucleated cells in the bone marrow and significantly decreased organ weights of thymus (P less than 0.001) and spleen (P less than 0.001) in female albino rats. Iron content, lipid peroxidation and superoxide dismutase activity of the liver and bone marrow were significantly increased as a result of benzene exposure. Prior administration of 6MFA, an interferon inducer with immunomodulating potential, was found to ameliorate some of the adverse effects of benzene as well as restoration of hepatic architecture histologically. Lipid peroxidation and iron content were both normalised, whereas superoxide dismutase activity was further increased and the number of lymphocytes and bone marrow cells returned to normal. Pretreatment of animals with 6MFA was able to enhance the SRBC antibody titre in benzene-treated immunosuppressed animals. The beneficial effects of 6MFA in the amelioration of the acute toxicity of benzene therefore assume certain significance.

Animals↗