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Biomedical subjects

S V Chandra

Publications and source records attributed to S V Chandra.

At least 55 records · Page 3Linked to original sources
PubMed1987

Possible role of regional superoxide dismutase activity and lipid peroxide levels in cadmium neurotoxicity: in vivo and in vitro studies in growing rats.

Cd2+ (0.4 mg/kg) administration to growing rats (45 +/- 5 g) intraperitoneally, daily for 30 days was found to decrease the activity of superoxide dismutase (SOD) in all the brain regions, except hippocampus. The concentrations of lipid peroxides were significantly elevated in the cerebellum, cerebral cortex, corpus striatum and midbrain. A 100% inhibition in SOD activity was observed by 14 microM and 50 microM of Cd2+ in bovine blood and rat brain preparations, respectively. Cadmium-induced strong inhibitory effect on brain and purified bovine blood SOD suggested a direct effect of the metal on enzyme molecule. Furthermore, in vitro addition of a wide range of Cd2+ (1-100 microM) increased the rate of lipid peroxidation (LPO) reaction in fresh brain homogenate, however, did not affect boiled homogenate. The studies on LPO in reconstituted homogenate resulting from mixing of fresh and/or heated different subcellular fractions indicated the presence of some heat-labile Cd2+ -sensitive factor in 15000 x g pellet fraction. It is suggested that Cd2+ directly and indirectly through inhibition of SOD, increases the LPO of cell membranes and thus produces damage to the associated physiological functions leading to central nervous dysfunctions.

Animals↗
PubMed1987

The combined effect of Pb2+ and Mn2+ on monoamine uptake and Na+, K+-ATPase in striatal synaptosomes.

Rat striatal synaptosomes (P2-fraction) were subjected to lipoperoxidation by the addition of 120 microM Fe2+ and 200 microM ascorbic acid. This preparation (pretreated synaptosomes) was used to investigate the interaction of Pb2+ and Mn2+ on the uptake of tritiated catecholamines, Na+, K+-ATPase activity and malondialdehyde (MDA) formation in order to understand the mechanism of enhanced neurotoxicity by concurrent exposure to these metals. The combination of Pb2+ and Mn2+ (25 microM + 100 microM, respectively) produced a significant increase in the uptake of 3H-Dopamine only in the untreated synaptosomes. No significant effect was noted on the uptake of 3H-Norepinephrine in either pretreated or untreated synaptosomes. However, the combination of Pb2+ and Mn2+ produced a pronounced decrease in the activity of Na+, K+-ATPase, but the magnitude of the change was the sum of the individual metal effects. Metal interaction did not produce any significant change in the formation of MDA compared to the control (without addition of metals). These results indicate that Pb2+ and Mn2+ interaction may produce inhibition in the activity of transport ATPase in both the preparation of synaptosomes, with more pronounced effect of synaptosomes subjected to lipoperoxidation and these changes may be responsible for the disruption in the physiology of nerve impulse transmission.

Animals↗
PubMed1987

The effect of lead exposure on the testis of growing rats.

Daily intraperitoneal administration of lead (8 mg/kg) as lead acetate in male rats from 21 till 120 days of age triggered histopathological and biochemical alterations in the testis. Histopathological examination revealed disturbance in spermatogenesis besides Leydig cells degeneration. There was an increase in cholesterol, decrease in ascorbic acid contents and reduction in the glucose-6-phosphate dehydrogenase activity in the testis of lead-treated rats. These alterations suggest that the disturbed steroidogenesis during growing stage may be responsible for altering the germinal function of the testis at maturity.

Animals↗
PubMed1987

Effects of cadmium on superoxide dismutase and lipid peroxidation in liver and kidney of growing rats: in vivo and in vitro studies.

Intraperitoneal administration of cadmium acetate (Cd2+, 0.4 mg/kg) to rats daily for 30 days was found to inhibit the activity of superoxide dismutase (SOD), to increase the endogenous levels of lipid peroxides and lipid peroxidation in the liver and the kidney tissues. Addition of varying concentrations of Cd2+ (10-100 microM) in vitro also inhibited SOD in both the tissues. It appears that the inhibition of SOD could be due to direct interaction of Cd2+ with the enzyme molecule. Lipid peroxidation reaction was also increased after addition of Cd2+ to fresh homogenate of these tissues, however, it did not produce any effect in heated homogenates in in vitro experiments. It indicated that Cd-induced elevation in lipid peroxidation may not be only due to the possibility of higher level of superoxide radicals resulting from inhibited superoxide dismutase but could also be as a result of direct action of Cd2+ on the peroxidation reaction. Thus, the possibility of involvement of free radical damage to the membrane structures in Cd toxicity has been demonstrated in these experiments.

Animals↗
PubMed1986

The action of thallium acetate on phasic transmitter release in the mouse neuromuscular junction.

Endplate potentials (EPP's) and miniature endplate potentials (MEPP's) were recorded from neuromuscular junctions of the mouse phrenic nerve-diaphragm preparation, blocked by high Mg++ (12 X 10(-3) mol/l)-Ringer. Superfusion of the preparations with Mg++-Ringer solutions containing thallium acetate (5 X 10(-4) mol/l Tlac) decreased phasic transmitter release as judged by EPP amplitudes as well as average quantal content, until total synaptic blockade (within about 300 min) occurred. Simultaneously MEPP amplitudes remained unchanged, whereas the frequency of MEPP's increased. When EPP amplitudes and/or quantal content were reduced by 50% (usually within about 180 min), superfusion with Mg++-Ringer solution without Tlac did not restore phasic transmitter release. However, the increase in spontaneous transmitter release was reversible, as MEPP frequencies returned to normal values. 4-Aminopyridine (5 X 10(-4) mol/l 4-AP) as added to the bath solution in the state of 50%-reduced phasic release temporarily restored EPP amplitudes and average quantal content, whereas MEPP amplitudes remained unchanged. It is concluded that thallium irreversibly blocks phasic transmitter release, whereas spontaneous transmitter release is reversibly enhanced.

4-Aminopyridine↗
PubMed1986

Endosulfan induced inhibition of 3H-5-hydroxytryptamine uptake in platelets.

Endosulfan, a chlorinated pesticide, is widely used to control various insect pests. Rats exposed to 1 mg and 3 mg endosulfan/kg for periods of 10, 30, and 60 days showed significant (P less than 0.05) inhibition of [3H]5-hydroxytryptamine (5-HT) uptake by platelet-rich plasma (PRP) in an ex vivo study. Rats treated with endosulfan (1 and 3 mg/kg) up to 60 days elucidated a marked inhibition of ADP-induced aggregatory responses of the platelets. Incubation of PRP with 10 microM and 100 microM endosulfan for 15 min at 37 degrees C also resulted in significant (P less than 0.05) inhibition of platelet aggregation in vitro. The paper discusses the use of rat blood platelets as a model for the study of neuro- and cardiovascular toxicity of endosulfan.

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↗
PubMed1985

The effect of substrate and potassium on the inhibitory kinetics of MnCl2 on the enzyme K+-p-nitrophenyl phosphatase in rat brain.

The effect of Mn2+, a divalent metal, on the enzyme K+-p-nitrophenyl phosphatase (K+-PNPPase) was studied in rat brain. The metal was found to be a moderate inhibitor of the enzyme, with an I50 of approximately 480 microM. The inhibition was pH dependent, but not temperature dependent. On measurement of the inhibition with varying concentrations of PNPP (1-5 mM), the I50 value remained constant. However, when the inhibition was measured with K+ (5-20 mM), the I50 value increased from 130 microM to 490 microM, suggesting that K+ antagonized the effect of Mn2+. In kinetic studies, Mn2+ inhibited the enzyme in a non-competitive manner with respect to PNPP. The Km remained constant (2.9), but the Vmax was decreased from 5.0 to 1.6. However, with respect to K+, the inhibition was competitive, as the concentration for half maximal activation (K0.5) increased from 1.3 to 8.9 mmol l-1 with 1 mM of MnCl2, suggesting that the apparent affinity of K+ for the enzyme was decreased. The apparent Vmax was not affected. The degree of cooperactivity (n) measured as the slope of the Hill plot remained unaltered (1.9 +/- 0.2) over the entire concentration range of MnCl2 tested.

4-Nitrophenylphosphatase↗
PubMed1985

Biogenic amines and some metals in brain of cadmium-exposed diabetic rats.

Diabetic rats (alloxan diabetes) were exposed to cadmium (2 mg kg-1 i.p.) daily for 21 days to investigate the levels of blood glucose, biogenic amines and iron, copper, zinc and cadmium in the brain. Cadmium exposure to diabetic rats produced a significant exacerbation in the hyperglycemic effect and accumulation of cadmium in the blood compared with that observed after diabetes or cadmium exposure alone. The elevation in the levels of brain dopamine and 5-hydroxytryptamine were also more pronounced in cadmium-exposed diabetic rats compared with either cadmium exposure or diabetes alone. Cadmium exposure to diabetic rats also produced significant changes in the concentrations of copper in the blood. These results indicated enhanced cadmium toxicity in diabetic rats.

Animals↗
PubMed1985

The effects of some divalent metals on cardiac and branchial Ca2+-ATPase in a freshwater fish Saccobranchus fossilis.

The heart and gill of a freshwater fish Saccobranchus fossilis have been shown to contain a Ca2+-activated ATPase involved in Ca2+ transport. Enzyme showed optimal activity at 3 mM Ca2+ and 3 mM ATP for gills and at 3 mM Ca2+ and 1 mM ATP for heart. Mg2+ was equally effective in stimulating enzyme activity but was not essential for hydrolysis. Maximum activity was found in heart ventricular muscles as compared to gills. Among all the metals tested Hg2+ was the most toxic (IC50, 0.75 and 0.85 microM for heart and gill, respectively) followed by Pb2+, Mn2+, and Cd2+. The inhibition was concentration dependent and reached almost 100% with each metal at the highest concentration. Stimulation of enzyme activity was observed at lower concentrations of Mn2+ and Cd2+ but not with Pb2+ and Hg2+. Stimulation was more pronounced with Mn2+ than with Cd2+ in both heart and gills. The results indicated that the inhibitory effect of these metals might be through the Ca2+-ATPase which is a manifestation of the calcium pump in various tissues.

Animals↗
PubMed1985

Role of neurotransmitters in endosulfan-induced aggressive behaviour in normal and lesioned rats.

Normal and lesioned rats exposed to 3 mg/kg i.p. endosulfan for 10 subsequent days showed elevated foot-shock fighting behaviour in septal and nigral brain-lesioned animals. Increased ipsilateral circling was noticed in unilateral-nigral lesioned rats. A marked decrease in locomotor activity and no seizure pattern were recorded in rats treated with chlorpromazine (CPz). Electroencephalographic recording on the tenth day of endosulfan exposure showed high-voltage slow activity (HVSA) with occasional spindles and 5-6 Hz amplitude of 200 microV. In the treated rats an increase in the concentration of dopamine (DA) and a decrease in serotonin (5-HT) were recorded in amygdaloid, septal and nigral brain-lesioned rats.

Aggression↗