Toxic Effects of Aluminium on Female Reproductive System in Presence of Ethanol Coexposure

Abstract

Both aluminium and ethanol are pro-oxidants and toxic. Uncontrolled use of aluminium and increasing trends of ethanol consumption in India increased the chance of coexposure to aluminium and ethanol. There are possibilities, that both of them follow common mechanisms to produce reproductive toxicity. The present study was planned to identify the effects of aluminium administration on the microscopic structure of ovary and to clarify any possible protection conferred by the concomitant administration of ethanol. Sixteen female rats divided into one control and three experimental groups exposed to aluminium (4.2mg/kg body weight) and ethanol (1gm/kg body weight) for 3 months. After the exposure period, ovaries were processed for light microscopic examination. Ovary showed significant atretic follicles with degenerated ova and vacuolation. Rupture of zona pellucida in oocyte seen in aluminium treated animals. Ethanol treated group showing absence of growing follicles, increased large corpora lutea. Dilated and congested vessels were observed in the growing follicle. The effects of combined administration of aluminium and ethanol treated groups showed with acute degeneration of growing follicles, with desquamation of pyknotic granulosa cells and degenerated oocyte. Multiple vacuoles of degenerated granulosa cells with dilated congested vessels and edema seen. Hyaline material seen inside the degenerating follicles. It has been suggested that the ethanol induced augmentation of impacts of aluminium on the Ovary.

The antioxidant/anti‐inflammatory protective effects of rutin against ethanol‐induced testicular perturbation in rats: Involvement of the immunosuppressive indoleamine 2,3‐dioxygenase

“…5,39,40 Our study is in agreement with the previous report by demonstrating a diminution in antioxidant enzymes, an increase in inflammatory biomarkers and LPO following EtOH exposure. Alteration in the histo-architecture due to EtOH exposure in the testicular microenvironment was earlier reported 41 due to OS, LPO and inflammation. Histological results in the present study indicated that EtOH exposure elicited moderate degeneration of the Sertoli cells and the necrotic appearance of the Leydig cells.…”

Effects of ethanol on testis: A histopathological study in adult rats

“…Hence, ethanol-induced elevation of germ cell apoptosis and necrosis and suppression of cell proliferation may contribute to testicular atrophy. 28 These effects were observed in the reduced tubular diameter and cross-sectional areas of the treated animals. However, when the animals were co-exposed to both ethanol and aluminium, the vacuolar-degenerative changes appeared in the cytoplasm of the spermatogenic epithelium and in the sertoli cells and abnormal distribution of spermatozoa in the Lumina.…”

The Detrimental Effects of Alcohol Consumption on Infertility of Humans and Laboratory Animals: A Review

“…According to the study, there was a lack of normal spermatogenic cell distribution in the seminiferous tubules, and some spermatocytes were fragmented in the lumen. The use of combined treatment of ethanol and aluminum via the oral route caused vascular degenerative alterations in the cytoplasm of spermatogenic epithelium and Sertoli cells in testes (Ghosh et al, 2021a).…”

“…Exposure to pro-oxidants and toxic chemicals, such as aluminum, can enhance alcohol toxicity (Ghosh et al, 2021a). The microscopic structure of the testes was identified using a three-month-experimental study with 16 male rats, including three treatments and one control group.…”

“…The impaired reproductive function of female rats exposed to ethanol and aluminum for 3 months has been previously reported. The alcohol and aluminum exposure groups indicated ovarian damage and vacuolation, split of the zona pellucida, limited follicular development, decreased corpora lutea, and obstruction of blood arteries in the developing follicle (Ghosh et al, 2021b). Alcohol administration also inhibited the surge in proestrus Luteinizing hormone (LH) and ovulation in female rats.…”