No abstract

Infertility is a major health issue affecting human life. The most notable factors causing male infertility is exposure to environmental contaminants. Bisphenol A (BPA) is a common toxic environmental contaminant. Human population is exposed to bisphenol A through air, water, food and a variety of industrial products. Growing evidence from research on laboratory animals supports the hypothesis that bisphenol A is able to adversely affect male reproductive function. The specific mechanisms of action of bisphenol A are wide but not definite. Bisphenol A interferes with the hormonal metabolism and regulation, binding affinity or enzymatic activity, resulting in a deviation from a normal reproductive behaviour. Binding ability to androgen and oestrogen receptors, as well as other properties, is currently investigated. A decreased sperm count, inhibition of sperm motility and reduction of organ weights were observed and linked with oxidative stress after bisphenol A treatment. In addition, prenatal exposure to bisphenol A may lead to adverse effects in the offspring. In this review, we address the topic of BPA effects on male reproductive function and emphasize its effects on testicular steroidogenesis and spermatogenesis. A considerably more detailed and systematic research focusing on bisphenol A toxicology is required for a better understanding of risks associated with exposure to this endocrine disruptor.

Nowadays, endocrine-disrupting chemicals are considered to be one of the main causes of the ever-increasing occurrence of problems with male fertility. These compounds of natural or anthropogenic origin are omnipresent in the environment and organisms are exposed to them practically nonstop through the air, water, food, and occupationally. Endocrine disruptors have the ability to mimic effects of reproductive hormones and demonstrably can interfere with the endocrine system leading to reproductive disorders at different levels, and considering male reproductive functions, most of the impacts are performed by the breakdown of estrogen-or androgen-mediated processes. A significant body of evidence based upon laboratory or wildlife animal experiments and metaanalysis of semen studies in men indicates that exposure to endocrine disrupting compounds is associated with male reproductive malfunctions, including impairment of spermatogenesis followed by reduced semen quality parameters (sperm concentration, motility, and morphology). Alkylphenols, bisphenol, and phthalates are substantial components of many products with which people come into contact daily. This brief review will emphasize on the possible effects of alkylphenols, bisphenol, and phthalates on the male reproductive system, and current research efforts related to these substances mainly in the context of two main processes taking place in testicular tissues-steroidogenesis and spermatogenesis.

In this study, the human H295R adrenocarcinoma cell line was exposed to different concentrations (0.04, 0.2, 1.0, 2.5 or 5 µg/mL) of nonylphenol (NP) to investigate its impact on the inhibition or induction of the steroid hormones production during 48 h of in vitro culture. The hormone production was measured using ELISA kits. Results of this in vitro study suggest various effect of nonylphenol in relatively low concentrations on the selected steroid hormones production by the human H295R adrenocarcinoma cell line. The inhibiting impact on progesterone and androstenedione production was observed. The amount of progesterone was significantly decreased at 1.0, 2.5 and 5 µg/mL NP. Equally, the androstenedione production significantly decreased at 5 µg/mL NP. On the other hand, the amount of testosterone and 17β-estradiol was induced after nonylphenol exposition. The significant increase of testosterone level was found out at treatment with 5 µg/mL NP. 17β-estradiol production significantly increased at the doses of 2.5 and 5 µg/mL NP.