Alcoholic beer consumption permute P21 and cyclin D1 expression, oxidative stress factors, and histomorphometric...

Ethanol consumption is increasingly prevalent in communities and has several side effects for humans. Chronic alcohol consumption is often associated with decreased libido and infertility. This study aimed to evaluate the impact of beer on spermatogenesis and proteins and gene expression of P21 and cyclin D1 in testicular tissue.

24 male mice were assigned to 4 groups; the Control group received normal saline, and the experimental groups received alcoholic beer (3 g/kg BW as 20% V/V). After 7, 15, and 35 days, mice were sacrificed, and a part of testicular tissues was stored at minus 70 ºC to measure the protein and gene expression of P21 and cyclin D1 by western blot and real-time PCR. Moreover, it measures the levels of malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT). Histomorphometry and histopathology were done.

The consumption of alcoholic beer led to increased protein and gene expression of P21 and decreased expression of cyclin D1, as well as reduced levels of SOD and CAT, increased levels of MDA, and subsequent tissue damage in the testicular tissue in a time-dependent manner. Also, the diameter of seminiferous tubules and the thickness of the germinal epithelium were increased in a time-dependent manner, and the percentage of seminiferous tubules with tubular differentiation, replacement, and negative spermiogenesis coefficients decreased significantly.

Alcoholic beer disrupted the process of cell division in the testes by reducing the expression of Cyclin D1, increasing p21 expression, and inducing oxidative stress, which in turn reduced sperm production and quality.