Effects of Acrylonitrile Toxicity in Female Ovary and Teratological Abnormalities in Mice

Acrylonitrile (ACN) is recognised for its carcinogenic and toxic properties, but its impact on female reproductive health in mammals is poorly understood. This study aimed to elucidate the chronic zoopathological effects of ACN on ovarian function and reproductive hormones in female albino mice (Mus musculus), and assess its teratogenic effects in offspring. A total of 70 female albino mice were randomly divided into three groups as follows: Group 1 (n=20) served as a negative control, Group 2 (n=20) administrated ACN at 10.17 mg/kg BW (1/10 of the oral ACN LD50) twice a week orally for 120 days, Group 3 (n=30) administrated the same dose of ACN three times a week orally for 120 days. On days 45, 90, and 120 after ACN exposure, blood samples were collected for to evaluate serum levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and oestradiol (E2) using enzyme-linked immunosorbent assay (ELISA) kits. After 120 exposure, Group 4 (n=12) were bred with adult males (n=6) to study teratogenic outcomes. The study found that there were significant reductions at all time points in LH, FSH, and E2 levels (P<0.05) of ACN-treated groups compared with the control, with Group 3 generally showing the lowest levels. Histopathological analysis revealed necrosis, cystic changes, apoptosis, and haemorrhage in the ovaries of Groups 2 and 3. Group 3 offspring exhibited multiple congenital defects including dwarfism, rough skin, limb malformations, and anotia. All neonates from this group died postnatally, exhibited body and tail abnormalities, and presented with kyphosis. In conclusion, ACN exposure significantly impairs reproductive hormone levels and ovarian morphology, leading to severe teratogenic effects. The results of this study indicate that ACN exposure has significant adverse effects on female reproductive function in mice, characterized by reductions in sex hormone levels, infertility, and teratological abnormalities in offspring.