Toxicity In Wistar Albino Rats Research Articles

Antioxidant Activities of Hydroalcoholic Extract of Ocimum sanctum Against Cadmium Induced Toxicity in Rats

The present study was undertaken to analyze the antioxidant (both enzymic and nonenzymic) activities of leaves of Ocimum sanctum hydroalcoholic extract against cadmium induced damage in albino rats. Oral administration of cadmium as CdCl(2) (6.0mg/kg body weight) led to significant elevation of lipid peroxidation (LPO) levels and significantly decreased Superoxide Dismutase (SOD), Catalase (CAT), Glutathione Peroxidase (GPx), Reduced Glutathione (GSH) and Vitamin C (Ascorbate) levels. Administration of Ocimum sanctum extract (100mg/kg body weight, po) and (200mg/kg body weight, po) before and after cadmium intoxication showed a significant decrease in LPO levels and significant increase in SOD, CAT, GPx, GSH and Ascorbate levels. The results suggest that oral administration of Ocimum sanctum extract provides significant protection against cadmium induced toxicity in Wistar albino rats.

RETRACTED: Effects of leaves extract of Ocimum sanctum L. on arsenic-induced toxicity in Wistar albino rats

Therapeutic efficacy of oral administration of Ocimum sanctum (200mg/kg, once daily) post arsenic exposure (100 ppm in drinking water for 4 months) was investigated in rats. Animals exposed to arsenic (III) showed a significant inhibition of delta-aminolevulinic acid dehydratase (ALAD) activity, decrease in reduced glutathione (GSH) level and an increase in reactive oxygen species (ROS) in blood. On the other hand, a significant decrease in hepatic ALAD, and increase in delta-aminolevulinic acid synthetase activity were noted after arsenic exposure. These changes were accompanied by an increase TBARS level in liver and kidney. Activities of liver, kidney and brain superoxide dismutase and catalase also showed a decrease on arsenic exposure. Administration of O. sanctum post arsenic exposure, exhibited significant recovery in blood ALAD activity while, it restored blood GSH and ROS levels. Other blood biochemical variables remained unchanged on O. sanctum supplementation. Interestingly, there was a marginal, but significant depletion of arsenic from blood, liver and kidneys. The results conclude that post arsenic administration of O. sanctum has significant role in protecting animals from arsenic-induced oxidative stress and in the depletion of arsenic concentration. Further studies thus can be recommended for determining the effect of co-administrating of O. sanctum during chelating therapy with a thiol chelator.

(−)Epigallocatechin-gallate (EGCG) prevents mitochondrial damage in isoproterenol-induced cardiac toxicity in albino Wistar rats: A transmission electron microscopic and in vitro study

Altered mitochondrial function and free radical-mediated tissue damage have been suggested as important pathological events in isoproterenol (ISO)-induced cardiotoxicity. This study was undertaken to know the preventive effect of (−)epigallocatechin-gallate (EGCG) on mitochondrial damage in ISO-induced cardiotoxicity in male Wistar rats. Rats were pretreated with EGCG (30 mg/kg) orally using an intragastric tube daily for a period of 21 days. After that, ISO (100 mg/kg) was subcutaneously injected to rats at intervals of 24 h for 2 days. ISO-induced rats showed significant increase in mitochondrial lipid peroxidation products (thiobarbituric acid reactive substances and lipid hydroperoxides) and significant decrease in mitochondrial antioxidants (superoxide dismutase, catalase, glutathione peroxidase, glutathione- S-transferase, glutathione reductase and reduced glutathione). Also, significantly decreased activities of tricarboxylic acid cycle enzymes such as isocitrate, succinate, malate and α-ketoglutarate dehydrogenases and respiratory chain marker enzymes such as NADH-dehydrogenase and cytochrome- c-oxidase were observed in mitochondrial heart of myocardial infarcted rats. Prior treatment with EGCG (30 mg/kg body weight) significantly prevented these alterations and restored normal mitochondrial function. Transmission electron microscopic findings also correlated with these biochemical parameters. In vitro studies on the effect of EGCG on scavenging 1,1-diphenyl-2-picrylhydrazyl (DPPH ), 2,2′-azinobis-(3-ethyl-benzothiazoline-6-sulfonic acid) (ABTS +), superoxide anion (O − ), and hydroxyl (OH ) radicals also confirmed the free radical scavenging and antioxidant activity of EGCG. Thus, the observed effects are due to the free radical scavenging and antioxidant potential of EGCG. Thus, this study confirmed the preventive effect of EGCG on isoproterenol-induced mitochondrial damage in experimentally induced myocardial infarction in Wistar rats.