Prophylactic Effects of Melatonin in Lead Induced Toxicity in Rats

Authors

  • Mustafa Ghazi Alabbassi Department of Pharmacotherapy, College of Pharmacy, Al-Mustansiriya University, Baghdad, Iraq.
  • Saad Abdul-Rehman Hussin
  • Shatha Hussain Ali
  • Nazar Alwakeel

DOI:

https://doi.org/10.32947/ajps.v6i1.368

Abstract

Exposure to lead results in significant accumulation in most of vital organs, and free radical damage has been proposed as a cause of lead-induced tissue damage where oxidative stress is a likely molecular mechanism. This study is designed to evaluate therapeutic effects melatonin in lead-induced organs toxicity in rats.
Evaluation of melatonin in this respect was conducted in a rat model of lead-induced toxicity. All test groups here were challenged with subcutaneous injections of 100mg/kg lead acetate daily for one month. Melatonin in a dose of 20 mg/kg was administered intraperotoneal as adjunct treatment with lead
acetate. The changes in total body weight, weight of major organs (brain, liver and kidney), oxidative stress parameters, hemoglobin content, liver and renal functions, and histological appearance of the studied organs were evaluated and compared with that of negative and positive controls. In addition, melatonin has the ability to reverse the damage induced by lead in many organs and tissues through the reduction of MDA levels in RBCs, brain, liver and kidney; and the
increase in GSH levels in all studied organs; in addition to the improvement in the indices of the functions of the organs studied.
These findings demonstrate that melatonin capable of preventing damage of rat tissues caused by successive doses of lead acetate, and also demonstrate
that these animals had restored their organ functions due to treatment with melatonin

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Published

2009-06-01

How to Cite

Alabbassi, M. G., Hussin, S. A.-R., Ali, S. H., & Alwakeel, N. (2009). Prophylactic Effects of Melatonin in Lead Induced Toxicity in Rats. Al Mustansiriyah Journal of Pharmaceutical Sciences, 6(1), 157–173. https://doi.org/10.32947/ajps.v6i1.368

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