Estradiol treatment induces testicular oxidative stress and germ cell apoptosis in rats

Abstract

In order to understand the pathogenesis of estradiol induced effects in the seminiferous epithelium, studies were undertaken in adult rats with estradiol-3-benzoate administered for different durations. After 30 d of treatment, a significant rise in lipid peroxidation with concomitant fall in the activities of superoxide dismutase and catalase was observed. Both, serum and intra-testicular testosterone levels were found severely depleted. Seminiferous epithelium was devoid of elongated spermatids and spermatozoa by 30 d of treatment. Number of spermatocytes and round spermatids were significantly (p < 0.001) reduced. Flowcytometric analysis confirmed a drastic reduction of the haploid cell population (1c peak). Beginning from day 10 of treatment, there was a consistent rise in the number of pyknotic/apoptotic germ cells in the seminiferous epithelium. A gradual increase in Bax protein expression was observed with the duration of treatment. The shift in Bax immunostaining from the cytoplasm and nucleus of germ cells (at 10 d of treatment) to only nuclei of cells by 30 d of treatment was also noticed. By this time testicular tissue showed three-fold increase in caspase-8 enzyme activity. Viable testicular cells isolated in vitro decreased drastically subsequent to different periods of estradiol treatment. The above findings substantiate the fact that the testicular pathogenesis of estradiol benzoate treatment may be primarily because of altered reproductive hormone levels and high oxidative stress leading to germ cell apoptosis and subsequent germ cell loss in the seminiferous epithelium.

N-acetyl-l-cysteine modulates multiple signaling pathways to rescue male germ cells from apoptosis induced by chronic hCG administration to rats

“…Such alteration in the hormonal milieu induces hypospermatogenesis leading to reduced testicular weight in rodents. Chronic estrogen treatment results similar alterations in reproductive hormone levels that impairs spermatogenesis [32]. In the present study too, spermatogenesis is not completely arrested but impaired with significant reduction in the number of immature germ cells/tubule (Fig.…”

Involment of p53, Bax, and Bcl‐2 pathway in microcystins‐induced apoptosis in rat testis

“…For example, Maheshwari et al (2009) demonstrated that H 2 O 2 -elicited apoptosis of testicular germ cells is associated with activation of the p53, Bax, Fas/Fasl, and a simultaneous decrease in the Bcl-2 expression. It was also observed by Chaki et al (2006) that an elevated expression of cell death effector Bax may contribute to the rat germ cell apoptosis with estradiol-3-benzoate administered.…”

Assessment of Molybdenum Induced Alteration in Oxidative Indices, Biochemical Parameters and Sperm Quality in Testis of Wistar Male Rats

“…Rats treated with ammonium molybdate exhibited an increase in lipid peroxidation in the testis which could be due to concomitant increase in the generation of free radicals or reduced content/activity of antioxidants in testis. Reduced level of intratesticular testosterone might also be responsible for suppressed expression of antioxidant enzyme with a concomitant increase in peroxidative damage, disruption of spermatogenesis and an increase in germ cell apoptosis (Peltola et al, 1996;Chaki et al, 2006).…”