Molecular mechanisms underlying ameliorative impact of melatonin against age-dependent chronic arsenic toxicity in rats' brains.

Accumulation of random molecular damage such as oxidative DNA damage and inflammation is extremely found to be involved in the aging process. Due to extreme energy requirements and high lipid levels, the brain is more susceptible to oxidative damage during aging especially under exposure to toxic elements such as arsenic. Therefore, this study was aimed to evaluate the ameliorative effects of melatonin, as a neurohormone, on the arsenic-induced behavioral abnormalities, and the underlying mechanisms.

Melatonin: a pleiotropic hormone as a novel potent therapeutic candidate in arsenic toxicity.

Background: Arsenic is a natural element which exists in the environment in inorganic and organic forms. In humans, the main reason for the toxicity of arsenic is its uptake via water sources. As polluted water and the problems associated with it can be found in many countries.

Attenuation of chronic arsenic neurotoxicity via melatonin in male offspring of maternal rats exposed to arsenic during conception: Involvement of oxidative DNA damage and inflammatory signaling cascades.

Prenatal exposure to arsenic is demonstrated to elevate the risk of brain damage and neurological disorders in the fetus, mainly due to its ability for crossing through the placental barriers. Increase in oxidative stress, inflammation, and DNA damage is main mechanisms of arsenic-induced neurotoxicity. Therefore, this study aimed to evaluate the neuroprotective effects of melatonin, as a potent anti-oxidant and anti-inflammatory agent against arsenic toxicity in the brains of male offspring rats.