ABSTRACT
We have previously demonstrated that acute third ventricle injections of both lead and cadmium prevent the dipsogenic response elicited by dehydration or by central injections of dipsogenic agents such as angiotensin II, carbachol and isoproterenol in rats. We have also shown that the antidipsogenic action of cadmium may be due, at least in part, to activation of thirst-inhibitory central serotonergic pathways. In the present paper we show that in Wistar male rats the antidipsogenic effect of both lead acetate (3.0 nmol/rat) and cadmium chloride (3.0 nmol/rat) may be partially dependent on the activation of brain opiatergic pathways since central injections of naloxone (82.5 nmol/rat), a non-selective opioid antagonist, blunt the thirst-inhibiting effect of these metals. One hundred and twenty minutes after the second third ventricle injections, dehydrated animals (14 h overnight) receiving saline + sodium acetate displayed a high water intake (7.90 ñ 0.47 ml/100 g body weight) whereas animals receiving saline + lead acetate drank 3.24 ñ 0.47 ml/100 g body weight. Animals receiving naloxone + lead acetate drank 6.94 ñ 0.60 ml/100 g body weight. Animals receiving saline + saline drank 8.16 ñ 0.66 ml/100 g body weight whilst animals receiving saline + cadmium chloride drank 1.63 ñ 0.37 ml/100 g body weight. Animals receiving naloxone + cadmium chloride drank 8.01 ñ 0.94 ml/100 g body weight. It is suggested that acute third ventricle injections of both lead and cadmium exert their antidipsogenic effect by activating thirst-inhibiting opioid pathways in the brain
Subject(s)
Animals , Male , Rats , Cadmium/antagonists & inhibitors , Cerebral Ventricles/drug effects , Drinking/drug effects , Lead/antagonists & inhibitors , Narcotics/pharmacology , Cadmium/pharmacology , Lead/pharmacology , Naloxone/pharmacology , Narcotic Antagonists/pharmacology , Rats, WistarABSTRACT
The study was carried out to find the preventive role of zinc on cadmium induced hepatotoxicity and involved 72 adult albino rats which were divided equally, at random, into three groups. Rats of the control group A were given saline subcutaneously. Rats of group B were given 1mg/kg body weight of cadmium chloride subcutaneously, daily for six weeks. The same dose of cadmium with an additional dose of 2 mg/kg body weight of zinc chloride was given subcutaneously, daily to 24 rats of group C for six weeks. All the rats were weighed weekly. Four rats of each group were sacrificed weekly and livers were processed for histological examination. Student's 't' test revealed a significant decrease in the mean body weight and increase in mean liver weight of rats of group B as compared to those of group C. Livers of group B showed progressive degenerative changes which ultimately resulted in fibrosis. These deleterious effects were prevented for only one week by zinc in livers of group C
Subject(s)
Animals, Laboratory , Zinc , Cadmium/toxicity , Liver/drug effects , Occupational Exposure , Cadmium/antagonists & inhibitors , Liver/anatomy & histology , Histological Techniques/methodsABSTRACT
Effect of zinc and cadmium on lipid peroxidation and catalase activity in liver, heart, brain and testis was determined in order to characterise the interaction of zinc with cadmium. Zinc and cadmium both increased lipid peroxidation significantly in the tissues studied. In animals pretreated with zinc prior to cadmium administration, significant decrease in lipid peroxidation in liver was observed. Lipid peroxidation was not affected significantly in testis but a significant increase was observed in heart and brain tissues. Catalase activity in testis increased significantly by zinc treatment with or without cadmium administration.