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Prospective protective role of melatonin against arsenic-induced metabolic toxicity in Wistar rats
Sudipta Pal1, Ajay K Chatterjee
1Biochemistry and Nutrition Laboratory, Department of Physiology, University of Calcutta, 92 Acharya Prafulla Chandra Road, West Bengal, Kolkata 700009, India.
Abstract:
Subchronic exposure to arsenic is associated with alteration of glucose homeostasis. Arsenic treatment (as sodium arsenite) of male Wistar rats (weighing 130-150 g) at a dose of 5.55 mg kg(-1) body weight (equivalent to 35% of LD(50)) (i.p.) per day for a period of 30 days produced hypoglycemia, with associated increased urinary excretion of glucose and depletion of liver glycogen and pyruvic acid contents. Mobilization of free amino acids from kidney to liver was facilitated by arsenic treatment. Arsenic exposure significantly decreased the glutamate-pyruvate transaminase activity in kidney. Glucose 6-phosphatase activity in liver tissue was also significantly decreased after arsenic treatment. In addition to these, liver lactate dehydrogenase activity was elevated due to arsenic treatment. Melatonin supplementation (i.p.) at a dose of 10 mg kg(-1) day(-1) for last five days prior to sacrifice reversed most of the above changes caused by arsenic. Melatonin, being a potent free radical scavenger may reduce arsenic-induced free radical production, and thereby, eliminating its toxic effects. So, arsenic-induced hypoglycemia, with associated glycogenolytic as well as glycolytic activities of liver can be partially counteracted by melatonin supplementation. Accordingly, it may be suggested that melatonin can serve as a prospective protective agent against arsenic-induced metabolic toxicity.
Insights
Subchronic arsenic exposure causes hypoglycemia and disrupts glucose metabolism in rats. Melatonin supplementation counteracted these toxic effects, suggesting its protective potential against arsenic-induced metabolic toxicity.
Area of Science:
- Biochemistry
- Toxicology
- Endocrinology
Background:
- Subchronic arsenic exposure is linked to disruptions in glucose homeostasis.
- Arsenic toxicity can manifest through various metabolic alterations.
Purpose of the Study:
- To investigate the effects of arsenic exposure on glucose metabolism in male Wistar rats.
- To evaluate the potential protective role of melatonin against arsenic-induced metabolic disturbances.
Main Methods:
- Male Wistar rats were administered sodium arsenite (5.55 mg/kg/day) for 30 days.
- Melatonin (10 mg/kg/day) was supplemented during the final five days of exposure.
- Key metabolic parameters including blood glucose, liver glycogen, urinary glucose, and enzyme activities were assessed.
Main Results:
- Arsenic exposure induced hypoglycemia, increased urinary glucose excretion, and depleted liver glycogen and pyruvic acid.
- Arsenic significantly altered glutamate-pyruvate transaminase and glucose 6-phosphatase activities, while increasing lactate dehydrogenase activity.
- Melatonin supplementation reversed most of the arsenic-induced metabolic changes.
Conclusions:
- Arsenic exposure significantly impairs glucose homeostasis and liver metabolism.
- Melatonin demonstrates a protective effect against arsenic-induced metabolic toxicity, likely through its antioxidant properties.
- Melatonin may serve as a potential therapeutic agent for mitigating arsenic's adverse metabolic effects.
