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Article

Effect of melatonin on arsenic-induced oxidative stress and expression of MT1 and MT2 receptors in the kidney of laboratory mice

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Pages 1216-1230 | Received 25 Dec 2018, Accepted 30 Dec 2018, Published online: 17 Jan 2019
 

ABSTRACT

Arsenic is a ubiquitous element of the environment present in both inorganic and organic forms. Arsenic exposure leads to oxidative stress and tissue damages in living organisms. Kidney is one of the major target organs that are affected by arsenic exposure. Besides its chronobiotic and immunomodulatory properties, melatonin plays an important role as an antioxidant and protects cells and tissues from oxidative damages. The aim of this study was to look over the effects of melatonin on arsenic-induced toxicity and MT1 and MT2 receptor expression in the kidney of mice. Healthy Swiss albino mice were used for this study. Experimental mice were received sodium arsenate (7 mg/kg B.wt./day) and melatonin (25 µg/100 g B.wt./day) alone and in combination for consecutive 30 days. Arsenic treatment increased malondialdehyde (MDA) level and suppressed the SOD and catalase activity in kidney tissue. Melatonin treatment to arsenic-treated mice suppressed the MDA level and restored the SOD and catalase activity in kidney tissues. Arsenic stress caused an increase in MT1 and MT2 receptor expression in kidney tissue. Melatonin supplementation to arsenic-treated mice maintained the increased expression of MT1 and MT2 receptors in kidney tissue. This finding may suggest the protective effect of melatonin and responsiveness of melatonin receptors during the arsenic-induced oxidative stress in kidney tissues of experimental mice.

Acknowledgements

Financial support from Council of Scientific and Industrial Research, New Delhi, and University Grants Commission, New Delhi, and help from establishment of State Biotech Hub, Tripura University, are gratefully acknowledged.

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This work was supported by University Grants Commission, New Delhi (Grant number 39-652/2010 (SR)) and Council of Scientific and Industrial Research, New Delhi (Grant number 37(1514)/11 EMR-II).

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