{'fraction_non_alphanumeric': 0.020594965675057208, 'fraction_numerical': 0.004576659038901602, 'mean_word_length': 5.336956521739131, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Zinc Toxicity to Aminergic Neurotransmitters in Rat Brain

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 (1/10 th 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.