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The effect of dietary selenium on lead neurotoxicity
Abstract:
Lead, when administered to male rats for 8 weeks in a dose of 20 mg/kg body weight, resulted in the impairment of the enzymes hexokinase and total ATPase in the cerebral and cerebellar regions of the brain. The changes were, however, more pronounced in the cerebellar region. Along with these, a decrease in acetylcholine esterase (AchE) and monoamine oxidase (MAO) was seen, thus affecting both cholinergic and adrenergic neurotransmitters. When selenium was administered concomitantly with lead, the values of total ATPase and hexokinase activities approached normal values in both brain regions. A significant improvement in acetylcholine esterase activity and MAO was also seen.
Insights
This study shows that lead exposure impairs brain enzymes like hexokinase and ATPase in rats. Selenium co-administration helped restore these enzyme activities, suggesting a protective effect against lead toxicity.
Area of Science:
- Neuroscience
- Toxicology
- Biochemistry
Background:
- Lead exposure is a significant public health concern, known to cause neurotoxicity.
- Enzyme function is crucial for neurotransmission and overall brain health.
- Understanding the protective mechanisms against heavy metal toxicity is vital.
Purpose of the Study:
- To investigate the effects of lead exposure on key brain enzymes in male rats.
- To evaluate the potential neuroprotective role of selenium against lead-induced biochemical changes in the brain.
Main Methods:
- Male rats were administered lead (20 mg/kg body weight) for 8 weeks.
- Activities of hexokinase, total ATPase, acetylcholine esterase (AchE), and monoamine oxidase (MAO) were measured in cerebral and cerebellar tissues.
- Selenium was administered concurrently with lead to assess its protective effects.
Main Results:
- Lead exposure significantly impaired hexokinase and total ATPase activities, particularly in the cerebellum.
- A decrease in acetylcholine esterase (AchE) and monoamine oxidase (MAO) indicated disruption of cholinergic and adrenergic neurotransmission.
- Concomitant administration of selenium normalized hexokinase and total ATPase activities and improved AchE and MAO levels.
Conclusions:
- Lead exposure induces significant biochemical alterations in the brain, affecting critical enzyme functions.
- Selenium demonstrates a notable neuroprotective effect, mitigating lead-induced neurotoxicity by restoring enzyme activities.