The present investigation envisages the toxic effects of aluminium on the cholinergic system of male albino rat brain. Aluminium toxicity (LD50/24 h) evaluated as per Probit method was found to be 700 mg/kg body weight. One-fifth of lethal dose was taken as the sublethal dose. For acute dose studies, rats were given a single lethal dose of aluminium acetate orally for one day only and for chronic dose studies, the rats were administered with sublethal dose of aluminium acetate once in a day for 25 days continuously. The two constituents of the cholinergic system viz. acetylcholine and acetylcholinesterase were determined in selected regions of rat brain such as cerebral cortex, hippocampus, hypothalamus, cerebellum, and pons-medulla at selected time intervals/days under acute and chronic treatment with aluminium. The results revealed that while acetylcholinesterase activity was inhibited, acetylcholine level was elevated differentially in all the above mentioned areas of brain under aluminium toxicity, exhibiting area-specific response. All these changes in the cholinergic system were subsequently manifested in the behavior of rat exhibiting the symptoms such as adipsia, aphagia, hypokinesia, fatigue, seizures, etc. Restoration of the cholinergic system and overt behavior of rat to the near normal levels under chronic treatment indicated the onset of either detoxification mechanisms or development of tolerance to aluminium toxicity in the animal which was not probably so efficient under acute treatment.
The present study was aimed to evaluate zinc toxicity to aminergic system in different areas of the brain of male albino rat, Rattus norvegicus. Zinc toxicity, evaluated as per Probit method was found to be 500 mg/kg body weight. For acute-dose studies, rats were given a single lethal dose of zinc chloride for one day only and for chronic-dose studies, the rats were administered with sub-lethal doses (1/10th of lethal dose) of zinc chloride every day for 90 days continuously. Various constituents of the aminergic system viz. dopamine, norepinephrine, and epinephrine and the catabolizing enzyme, monoamine oxidase (MAO) were determined in different regions of rat brain such as olfactory lobe, hippocampus, cerebellum, and pons-medulla on selected time intervals/days under acute and chronic treatment with zinc. The results revealed that while the levels of all aminergic neurotransmitters were elevated differentially in the above mentioned areas of brain, MAO activity registered nonsignificant inhibition in all brain regions under zinc toxicity. All these changes in the aminergic system were subsequently manifested in the behavior of rat exhibiting the symptoms of mild tremors, reduced locomotor activity and emotions, restlessness followed by lacrymation, salivation, etc. From these observations, it was obvious that zinc treatment caused severe perturbations in the functions of the nervous system. Restoration of the aminergic system along with behavior to the near normal levels under chronic treatment indicates the onset of detoxification mechanisms or development of tolerance to zinc toxicity in the animal which was not probably so efficient under acute treatment.
The present investigation has been conducted to study the effect of different sublethal concentrations of arsenic (5, 10 and 15 mg/L) on the muscle glycogen content in an Indian teleost, Clarias batrachus, during their post-spawning period (October to January).The species were exposed to various arsenic concentrations for six consecutive days i.e.,144 h. Significant differences in average muscle glycogen content were found in the treated male and female C. batrachus specimens. However, significantly higher (P < 0.01) muscle glycogen content was observed in male fish when compared to females in the untreated specimens. Arsenic caused muscle glycogenolysis in both sexes of C. batrachus. The depletions were not always dose (arsenic concentration) and time dependent, although higher concentrations were more glycogenolytic than the lower concentrations. After 96 h of treatment with arsenic, less depletion of muscle glycogen content was recorded in both sexes of fish.
The present investigation has been conducted to study of the effect of acute exposure of sublethal doses of arsenic tri-oxide (As(2)O(3)) on blood glucose level in an Indian teleost, Clarias batrachus, during their post-breeding season (October to January). The effect was correlated with the sex and doses used with time. Acute exposure of As(2)O(3) of 5, 10 and 15 mg/l for six consecutive days (i.e., 144 h) has been conducted on both sexes of C. batrachus. During the present investigation, it was noticed that the females were more reactive to arsenic in producing hyperglycemia compared to their male counterparts. The difference between males and females to produce hyperglycemia on exposure to arsenic appears to be dose dependent, as lower doses of 5 and 10 mg/l exhibit less difference between the two sexes compared to the highest dose order of 15 mg/l. After 96 h of treatment, a normoglycemic condition was observed in both sexes. However, no significant differences in average normal blood glucose levels were noticed in male and female C. batrachus during the post-breeding season.
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