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Biomedical subjects

S V Chandra

Publications and source records attributed to S V Chandra.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1990

Hypertension and myocarditis in rabbits exposed to hexachlorocyclohexane and endosulfan.

Male albino rabbits were exposed to the organochlorinated pesticides hexachlorocyclohexane (HCH) and endosulfan (2.5 and 5.0 mg/kg, ip) twice a week for 12 mo. The mean body weight of the rabbits at 12 mo was lower than that of the controls. There was rise in blood pressure and heart rate. Electrocardiograms (ECG) in both the exposed groups showed increases in PR, QT and RR intervals. Extensive myocardial damage was recorded with marked degeneration of muscle fibers vacuolization and leucocytic infiltration. Adrenals had thickened capsules and hyperplasia of cortical cells. Both pesticides produced significant increases (p less than 0.001) of 11-hydroxycortisone at all time intervals. Hypertension and myocarditis occurred in rabbits exposed to HCH and endosulfan.

Adrenal Glands↗
PubMed1990

Effect of chronic cadmium exposure on locomotor behaviour of rats.

Growing male rats were exposed to cadmium (Cd, 100 micrograms/kg, ip) for 51 days and the effect on the different components of locomotor behaviour was assessed on days 38, 46 and 51 of Cd exposure. Significant decrease in distance travelled, stereotypic time and movements, ambulatory time and vertical movements were observed in Cd-exposed rats, whereas the time of rest was increased. The number of entries into the inner as well as the outer squares and the total time spent in the inner squares of the floor area were significantly reduced. Results indicate that Cd exposure results in a general depression in all aspects of motor behaviour leading to decrease in gross locomotor activity. The involvement of an exaggerated emotional reactivity in the behavioural expression of the Cd-treated animals is also emphasized.

Acetates↗
PubMed1990

Role of aluminium in sporadic motor neuron disease.

In an attempt to ascertain the role of aluminium in sporadic motor neuron disease (MND), trace metals were estimated in blood, plasma and cerebrospinal fluid (CSF) of 38 patients of sporadic MND and 30 controls by direct current plasma emission spectrophotometry. CSF aluminium levels (20.76 +/- 4.38 micrograms/dl) were significantly higher (P less than 0.05) in those patients of MND who presented as progressive bulbar palsy (PBP) as compared to the other subtypes of MND (amyotrophic lateral sclerosis = 7.71 +/- 2.01 micrograms/dl; progressive muscular atrophy = 10.01 +/- 2.41 micrograms/dl) and controls (11.63 +/- 2.82 micrograms/dl). Aluminium may be important in the etiopathogenesis of a subgroup of sporadic MND.

Adolescent↗
PubMed1990

Therapeutic potential of thiamine hydrochloride in experimental chronic lead intoxication in goats.

The therapeutic potential of thiamine hydrochloride (vitamin B1) was evaluated in experimental chronic lead poisoning in goats. Eighteen goats divided into three groups were used. Goats of group A served as healthy controls while those of B1 and B2 received oral doses of 10, 15 and 20 mg lead acetate (5.43, 8.15 and 10.86 mg lead kg-1 body-weight) for 30, 30 and 31 days, respectively. At the end of the 91 days, thiamine hydrochloride was given at 20 mg kg-1 bodyweight subcutaneously for 15 days to group B2. Goats of group B1 served as lead exposed untreated controls. Significantly (P less than 0.05) higher lead concentrations were found in blood, liver, kidney and brain samples of lead exposed untreated goats than in healthy control or in lead exposed thiamine treated goats. The lead concentration, however, remained significantly (P less than 0.05) higher in all these tissues of thiamine treated goats than in healthy controls and no appreciable difference could be recorded in histopathological lesions between lead exposed untreated and thiamine treated goats.

Animals↗
PubMed1989

Cadmium toxicity and bioantioxidants: status of vitamin E and ascorbic acid of selected organs in rat.

Effects of i.p. administered cadmium acetate (Cd, 0.4 mg/kg) was studied on the levels of vitamin E and ascorbic acid in different brain regions, liver, kidney, testis, RBC and plasma at 15, 30 and 60 days intervals in male albino rats (45 +/- 5 g). Exposure to Cd for 15 days decreased the levels of vitamin E significantly in the liver and testis only, while 30 days of treatment resulted in a significant decline in cerebellum, cerebral cortex, corpus striatum, mid-brain + hypothalamus, and plasma. Cadmium administration for 60 days caused a decrease in vitamin E in all tissues. Furthermore, a duration-dependent decrease in hepatic ascorbic acid levels was noticed. The implications of these results are discussed.

Animals↗
PubMed1989

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

Normal and brain-lesioned (amygdala, septal and nigral regions) rats exposed to fenitrothion (10 mg/kg) for 15 subsequent days showed elevated foot-shock fighting behaviour (septal and nigral lesioned rats). Treated animals failed to perform the rotorod test and showed decreased locomotor activity followed by convulsions. The brain-lesioned rats treated with 10 mg/kg fenitrothion showed a marked decrease in the level of norepinephrine (NE) and serotonin (5-HT).

Aggression↗
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

Glutathione peroxidase and catalase in liver, kidney, testis and brain regions of rats following cadmium exposure and subsequent withdrawal.

Intraperitoneal administration of 0.4 mg/kg Cadmium (Cd) daily for 45 days was found to inhibit the activities of glutathione peroxidase and catalase in liver, kidney, testis and various brain regions at different time intervals. The magnitude of inhibition was increased with the period of exposure. Cd produced significant inhibition of glutathione peroxidase at 15 days in liver, kidney and cerebellum only; however, the enzyme activity was found to be decreased in all the tissues, except corpus striatum, at 30 and 45 days of exposure. Hippocampal glutathione peroxidase remained unaltered throughout the experiment. Catalase was found to be inhibited in all the tissues at different time intervals. The withdrawal of Cd treatment for 15 days after 45 days of exposure did not show significant recovery in the activity of both enzymes of different organs, except kidney and testis where partial and full recoveries respectively were observed. Since these two enzymes constitute an important part of cellular defence mechanism against oxidation, their widespread persistent inhibition may be of great significance in view of the recent reports showing the possible involvement of oxidative stress in the mechanism of Cd toxicity.

Animals↗
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↗
PubMed1988

Prevention of cadmium-induced effects on regional glutathione status of rat brain by vitamin E.

The effect of vitamin E on the cadmium-induced changes of glutathione metabolism was investigated in different brain regions. Daily intraperitoneal injection of cadmium (0.4 mg/kg) for 30 days significantly decreased the concentration of reduced glutathione (GSH), and the activities of glutathione reductase (GR) and glucose-6-phosphate dehydrogenase (GPDH) in the cerebellum, cerebral hemispheres and brain stem of rats. Cadmium elevated the levels of oxidized glutathione (GSSG) in cerebellum and cerebral hemisphere regions only, while the GSH/GSSG ratio decreased in all three brain regions. The only effect of intramuscular injections of vitamin E (5 mg/kg) given on alternate days for 30 days was a slight increase in GSH and GR in the cerebral hemispheres. The simultaneous administration of vitamin E and cadmium prevented cadmium-induced changes in GSH and GSSG levels and in the GSH/GSSG ratio, but the cerebellar GSH remained lowered. Furthermore, vitamin E, with the exception of GR in the cerebral hemispheres, did not prevent cadmium-induced changes in enzyme activities. As the simultaneous injections of vitamin E reduced cadmium-induced alterations in glutathione concentration without having any appreciable effect on the activity of related enzymes, it is suggested that the preventive effect of vitamin E is mediated through its antioxidative effect, saving GSH from oxidative destruction in the brain of cadmium-exposed rats.

Animals↗
PubMed1988

Glutathione status and cadmium neurotoxicity: studies in discrete brain regions of growing rats.

Intraperitoneal administration of cadmium (Cd2+, 0.4 mg/kg) daily for 30 days to rats was found to decrease the contents of reduced glutathione (GSH) and increase oxidized glutathione (GSSG) in various brain regions. These changes resulted in a significant decline in the GSH/GSSG ratio in different brain regions, except for the hippocampus and midbrain. In addition, the activities of glutathione reductase (GR) and glucose-6-phosphate dehydrogenase (GPDH) were also significantly inhibited in different brain regions. Measurement of regional Cd levels revealed that Cd administration significantly increased the levels in all brain regions except for the hippocampus, which could be the reason for not finding any change in any of the biochemical parameters studied in this region. The observed changes in the regional GSH/GSSG ratios could be the result of inhibition in GR activity, as this enzyme catalyzes an irreversible conversion of GSH to GSSG and is responsible for higher cellular GSH levels. GR uses NADPH in its reaction; therefore, the inhibition of GPDH may further aggravate the situation because of the short supply of NADPH. The alterations in the regional "glutathione status" may affect various related metabolic processes, including those required for detoxification of lipid peroxides which have recently been suggested to play a role in the mechanism of Cd neurotoxicity.

Animals↗
PubMed1988

Testicular effects of acrylonitrile in mice.

Daily oral administration of acrylonitrile (10 mg/kg body weight) to mice for a period of 60 days caused a significant decrease in the activity of testicular sorbitol dehydrogenase and acid phosphatase, and an increase in that of lactate dehydrogenase and beta-glucuronidase. Histopathological studies revealed degeneration of the seminiferous tubules. A decrease in the sperm counts of the epididymal spermatozoa was also observed in the animals of the acrylonitrile-exposed group. These observations suggest that acrylonitrile may affect the male reproductive function by causing testicular injury.

Acid Phosphatase↗