Melatonin abrogates nonylphenol-induced testicular dysfunction in Wistar rats

Abstract

Endocrine-disrupting chemicals present in the environment can bring about hormonal imbalance and be potentially harmful to the human health. Alkylphenols are omnipresent in the environment as they are constituents of several products. The aim of this study was to evaluate the effect of exogenous melatonin treatment on nonylphenol (NP)-induced oxidative stress and testicular toxicity in Wistar rats using biochemical and histopathological parameters. The oxidative stress biomarkers, activities of enzymatic and non-enzymatic antioxidants and histopathological evaluation were performed in testicular tissues. NP caused elevated TBARS levels and marked alteration of both nonenzymatic and enzymatic biomarkers. Furthermore, severe histopathological alterations were observed in the testis of NP-exposed animals as compared with that of the control rats. Melatonin supplementation ameliorated the alterations in these biochemical and histopathological variables in rats. In conclusion, our results demonstrated that melatonin through its antioxidant activity effectively protected against the NP-induced testicular toxicity.

Protective role of melatonin against adipose-hepatic metabolic comorbidities in experimentally induced obese rat model

“…In consonance with previous study, melatonin acts as a free radical scavenger that eliminates reactive oxygen and promotes the action and expression of endogenous antioxidants [ 26 , 57 ]. Our results are also consistent with a number of studies who have demonstrated anti-inflammatory, anti-proliferative and apoptotic properties of melatonin in experimental animals [ 58 – 60 ]. Nevertheless, the present results are not without limitations in such that the molecular mechanisms underlying the regulatory role of melatonin in obese animals, and the link between obestatin and other biochemical parameters were not investigated.…”

The effects of high‐fructose corn syrup consumption on testis physiopathology—The ameliorative role of melatonin

“…Furthermore, MLT has an excellent antioxidant property. Therefore, MLT can reduce the number of oxidative products such as hydroxyl, peroxyl radical, hypochlorous acid and singlet oxygen which cause cell damage (Tabassum, Parvez, & Raisuddin, ). The direct effects of MLT on male reproductive system have been investigated in animal experiments.…”

Ameliorative effect of Alpinia officinarum Hance extract on nonylphenol‐induced reproductive toxicity in male rats

“…Nonylphenol, an environmental contaminant, is known to have adverse effects on the mammalian reproductive system (Duan et al., 2016). NP deteriorative effects have been observed through disturbing testicular structure, spermatogenesis, reducing testis size and inducing oxidative stress (Tabassum et al., 2017). To the best of our knowledge, this study evaluated the effect of ALP extract on NP‐induced reproductive toxicity for the first time using nonenzymatic and enzymatic biomarkers of oxidative stress in the serum of male rats.…”

“…Several studies have demonstrated that NP causes reproductive dysfunction and enhances the production of reactive oxygen species (ROS) in the testis, liver and brain of animals (Kazemi et al, 2018; Kazemi, Feizi, et al, 2016; Kazemi, Mousavi Kani, et al, 2016). It has been evident that NP could reduce testis size, decrease circulating testosterone, disturb the testicular structure and suppress spermatogenesis (Tabassum et al., 2017; Ying et al., 2012). NP exposure decreased the lumen's diameter and epithelial thickness of seminiferous tubules leading to testicular atrophy (Jager et al., 1999).…”

“…Administration of NP increased H 2 O 2 production and lipid peroxidation while reduced antioxidant enzymes in the animals treated with NP (Chitra & Mathur, 2004). Different studies have pronounced vitamin E (Chitra & Mathur, 2004), melatonin (Tabassum et al., 2017) and honey (Shalaby & Saleh, 2011) as antioxidants that could ameliorate the oxidative damage caused by NP on the reproductive system.…”