PubMed Health⌕ Search

Biomedical subjects

R C Murthy

Publications and source records attributed to R C Murthy.

At least 37 records · Page 2Linked to original sources
PubMed1993

Aluminum ingestion alters behaviour and some neurochemicals in rats.

Effect of aluminum (Al) has been investigated on the brain of rats exposed to this metal (500 mg Al/liter in drinking water) daily for 180 days. A significant reduction in the spontaneous locomotor activity was noticed after 90 and 180 days of Al exposure to the rats, the magnitude of the change being almost identical at both the time intervals. Aluminum exposure also produced significant deficits in acquisition and retention of learned response in active avoidance situation, these changes being time dependent. A significant retardation of the extinction of the learned task was noted in Al exposed rats especially at 180 days. There was significant increase in the lipid peroxidation and decrease in the activity of Mg(2+)-ATPase and Na+,K(+)-ATPase in the brain of rats at 180 days after Al exposure. The increase in the contents of the metal was maximum in rest of the brain region (87% of control) followed by hippocampus and cerebral cortex (59% of controls), cerebellum and corpus striatum (43% and 44% of controls, respectively) after 180 days. Whether Al is responsible to initiate neurotoxic effects by producing changes in the structure and function of the plasma membrane needs further investigations.

Adenosine Triphosphatases↗
PubMed1992

Effect of zinc on immune functions and host resistance against infection and tumor challenge.

The effect of zinc treatment on immune function and resistance against infection and tumor challenge was studied in mice. Swiss albino mice were treated with zinc acetate (3 mg/kg body weight) in one or two intraperitoneal injections. Various immune function assays were performed in treated animals. Zinc treatment to normal animals caused potentiation of T-lymphocyte and macrophage functions. Zinc treatment was also found to increase host resistance against Candida albicans and Semliki Forest virus infections. Increased resistance against endotoxin shock and Ehrlich's ascites tumor challenge was also observed in zinc treated animals. It can be stated from this study that zinc treatment potentiates the cell mediated immunity and host resistance against infection and tumor challenge.

Animals↗
PubMed1991

Ultrastructural observations in testicular tissue of chromium-treated rats.

The administration of hexavalent chromium (2 mg/kg, ip as potassium dichromate) in adult rats daily for 15 days produced significant increases in the blood and testicular chromium levels. Although no light microscopic pathologic changes or alterations in epididymal sperm counts and motility were observed, lanthanum perfusion in treated rats revealed leakage of Sertoli-cell tight junctions under EM. A few tubules showed marked ultracellular alterations in the form of vacuolization of cytoplasm and degeneration of mitochondria in the epithelial cells. Late stage spermatids were the most affected germ cells. The mitochondrial sheath of the midpiece was vacuolated, incomplete, swollen, or broken in places. The observed alterations may result in the disruption of normal testicular physiology leading to reproductive impairment after chromium exposure.

Animals↗
PubMed1991

Lead-induced fetal nephrotoxicity in iron-deficient rats.

Lead administration (250, 500, 1000, and 2000 ppm, as lead acetate) in drinking water during fetal development (from 15 to 20 days of gestation), in normal and iron-deficient pregnant rats, revealed dose-dependent increases in the lead content of maternal blood that was more marked in iron-deficient animals. The placentae and fetuses did not show a dose-dependent increase in lead content. Lead administration revealed dose-dependent hydropic degeneration of renal proximal cells in the fetuses. The highest dose (2000 ppm lead) and iron deficiency exhibited more lead accumulation in maternal blood, placentae, and fetuses, and maximum pathologic changes in the fetal kidney when compared with the other doses and also with the fetuses of dams not deficient in iron.

Animals↗
PubMed1991

Lead induced ultrastructural changes in the testis of rats.

Oral lead administration (250 ppm lead acetate through drinking water) to weaning male rats for 70 days resulted in the marked accumulation of this metal in blood and testicular tissue. No marked changes were evident in light microscopy. Ultrastructural changes were revealed in the form of vacuolisation of Sertoli cell cytoplasm and increase in the number and size of lysosomes. Some of the vacuoles contained vesicle like structures. Although there was no impairment of spermatogenesis, the changes in the Sertoli cells may lead to changes in spermatogenesis after chronic exposure.

Administration, Oral↗
PubMed1991

Cardiotoxicity and hypertension in rats after oral lead exposure.

The rats were exposed to lead (0.25, 0.5 and 1.0 per cent lead acetate through drinking water) for 90 days to study its effect on some physiological and morphological parameters of the cardiovascular system. Blood lead levels increased in a dose dependent manner but heart tissue showed rise at only two higher doses in exposed animals. The two higher doses of lead resulted in an increased arterial blood pressure and calcium influx in atrial trabeculae and papillary muscles. No marked pathological or histochemical changes were observed in heart tissue excepting congestion and slightly reduced activity of succinic dehydrogenase in the highest dosed group. It was concluded that lead exposure through drinking water may produce increased arterial blood pressure and minor changes in the myocardium. Whether these changes are mediated through the effect of lead on the calcium transport needs further investigation.

Administration, Oral↗
PubMed1991

Ultrastructural changes in rat lungs exposed to combinations of cadmium, zinc, copper, and nickel.

The morphological effects of single intratracheal intubation of cadmium oxide (CdO) with oxides of zinc (Zn), copper (Cu), and nickel (Ni) at their threshold limit values on alveolar macrophages and type II cells were studied. The combinations used were: CdO + ZnO (0.1 mg + 5.0 mg); CdO + CuO (0.1 mg + 0.2 mg); and CdO + NiO (0.1 mg + 1.0 mg). Rats sacrificed after one week recovery period showed distinct morphological changes. Alveolar macrophages and type II cells exposed to CdO and ZnO showed an increase in number, shape, and size of vacuolar phagolysosomes. Multivesicular bodies and lamellar bodies were also seen, as well as the lack of distinct nucleoli. The CdO/CuO combination showed an increase in the number of dense vacuolar phagolysosomes and large aggregates of multivesicular bodies. Hypertrophy of mitochondria was also evident in this combination. The CdO/NiO combination showed more distinctive changes compared to the other two combinations in lysosomes, membranous whorls, multivesicular bodies, residual bodies, and number of mitochondria. Our findings using combination exposures of CuO and ZnO with CdO indicate the existence of competitive inhibition resulting in some form of protective action. On the other hand, the CdO/NiO exposure seemed to be additive showing structural modifications, premature aging, faster degeneration, and release of abnormal membrane structures.

Animals↗
PubMed1990

Effect of hexavalent chromium on testicular maturation in the rat.

Daily intraperitoneal administration of hexavalent chromium (Cr6+; 1, 2, and 3 mg/kg intraperitoneally as potassium dichromate) in weaned rats for an entire duration of 55 and 90 days of age produced dose- and duration-dependent enzymatic and pathologic alterations. At 55 days, the pathologic changes were not seen in testes of Cr6+ treated rats, but the activities of sorbitol dehydrogenase, lactic dehydrogenase, gamma-glutamyl transpeptidase, and glucose-6-phosphate dehydrogenase were significantly altered. When the treatment was prolonged to sexual maturity, that is, 90 days of age, the alterations in enzyme activities were greater, and there were dose-dependent pathologic changes in the testes of Cr(6+)-treated rats. These alterations suggest a risk to growing testes if rats are exposed to Cr6+ during the prepubertal stage of development, which, in turn, may disturb normal testicular physiology at adulthood.

Animals↗
PubMed1990

Comparative neurotoxicity of cadmium in growing and adult rats after repeated administration.

The effect of cadmium administration (Cd 0.4 mg/kg, ip, intraperitoneally, daily for 30 days) on its accumulation, contents of 5-hydroxytryptamine (5-HT) and 5-hydroxyindole acetic acid (5-HIAA) in different brain regions in growing and adult rats was investigated. Cadmium was found to significantly increase the levels of 5-HT and 5-HIAA in all the brain regions of adult rats while the levels of 5-HT and 5-HIAA were significantly decreased in most of the brain regions of growing rats. The accumulation of cadmium in all the brain regions was significantly more marked in growing rats compared to adults after identical exposure. In conclusion, there was an age difference in both the accumulation of cadmium and 5-HT turnover in the brain regions. However, the regional neurochemical changes were not correlated with the magnitude of cadmium accumulation in both the groups.

Aging↗
PubMed1989

Embryotoxicity and fetotoxicity of orally administered hexavalent chromium in mice.

The embryotoxic and fetotoxic potential of hexavalent chromium (Cr+6) in mice was investigated by administering 250, 500, and 1000 ppm of potassium dichromate daily through drinking water during the entire gestation period. An increase in embryonic deaths was observed; however, in the mothers treated with the highest dose, there was complete absence of implantation sites. No major abnormality was observed in the fetuses except that Cr+6 exposure increased the incidences and types of external and skeletal malformations. It is concluded that oral exposure to Cr+6 causes dose-dependent embryolethal effects in mice.

Abnormalities, Drug-Induced↗
PubMed1989

Lead induced testicular changes in protein malnourished rats.

The effect of concurrent low protein (8% casein) diet and lead (Pb) exposure (1 mg/ml lead acetate in drinking water) on testes of weaned rats up to 90 days of age was investigated Histopathological examination of testes of lead treated rats maintained on low protein diet revealed marked pathological changes associated with greatly reduced succinic dehydrogenase, glucose-6-phosphate dehydrogenase and adenosine triphosphatase activity as revealed histochemically compared to lead treated rats fed normal protein diet. It was concluded that higher accumulation of lead may be responsible for altering the enzyme levels and inducing the testicular degeneration to a greater extent in low protein fed rats compared to their counterpart controls.

Animals↗
PubMed1989

Zinc protects testicular injury induced by concurrent exposure to cadmium and lead in rats.

The effect of coexposure to lead and cadmium (each 50 ppm alone and 25 ppm in combination) on the testes of rats and the preventive role of zinc (50 ppm) was investigated by administering these metals through drinking water. Male weaned albino rats were exposed to these metals for 120 days. Testicular histology, sperm counts and sperm motility were studied in these rats. The animals coexposed to lead and cadmium exhibited much more pronounced pathological changes and reduced sperm counts compared to the animals exposed to either of the metals alone. Zinc supplementation to the lead + cadmium exposed rats revealed the protective effect of zinc on these parameters. The observed higher magnitude of changes in the testes of lead + cadmium exposed group seems to be due to the excessive cadmium accumulation.

Animals↗
PubMed1989

Chronic cadmium-ethanol administration alters metal distribution and some biochemicals in rat brain.

The effects of cadmium (100 ppm through drinking water) and ethanol (5 g/kg by gastric gavage) administration on biogenic amines, metal distribution and certain enzymes in rat brain was investigated after 90 days of exposure. Co-exposure group revealed significant accumulation of cadmium and also increase in zinc levels compared to all the other groups. Ethanol alone decreased MAO activity and increased NE and 5-HT level while in combination with Cd, these effects were more magnified. It is, therefore, suggested that the persons consuming alcohol may be more prone to the neurotoxic effects of this metal.

Animals↗
PubMed1989

Effect of manganese on some bioantioxidants in various organs of protein-deficient rats.

The effect of manganese exposure (Mn2+ 4 mg Mn/kg intraperitoneally) on certain bioantioxidants in brain, liver, kidney and testes in growing rats maintained on 21% and 8% casein diet were investigated. Manganese administration for 30 days caused significant reduction in the level of GSH (reduced glutathione) in liver and testes and GR (glutathione reductase) and G-6-PDH (glucose-6-phosphate dehydrogenase) in brain, liver and testes. The magnitude of alteration was greater in 8% casein diet fed animals compared to rats maintained on 21% casein diet. These results indicate that protein deficient animals are more susceptible to the manganese induced biochemical changes in various tissues. The mechanism of such changes is discussed.

Animals↗
PubMed1986

Embryotoxic and teratogenic effects of interaction of cadmium and lindane in rats.

Embryotoxic and teratogenic effects of cadmium and lindane were studied in rats. Cadmium or lindane alone did not produce any significant malformations in the 20 day old foetuses whereas their combination caused significant reduction in the body weight of dams and pups and increased total embryonic deaths. Skeletal deformities like wavy ribs, reduced skull ossification and reduced caudal vertebrae were potentiated in coexposure group. The study indicated that the simultaneous exposure to cadmium and lindane may have more deleterious effects on the developing foetus compared to either alone.

Abnormalities, Drug-Induced↗