Exposure to arsenic causes health problems and is associated with adverse effects on fertility and development. Humans are facing increasing exposure to arsenic from multiple sources, such as drinking water, food products, and industrial processes. The mechanisms behind arsenic-induced reproductive toxicity and its impact on fertility and the development of future generations are investigated by the protective role of metformin (200 mg/kg) against arsenic-induced (20 ppm AsO) ovarian damage in both maternal and offspring generations. Results showed arsenic exposure caused significant weight loss, increased mortality, reduced serum anti-Mullerian hormone (AMH) levels, and heightened oxidative stress, indicated by increased reactive oxygen species (ROS), malondialdehyde (MDA), and reduced ovarian antioxidant activity. Gene expression changes related to apoptosis and inflammation, such as BAX, Bcl-2, Bcl-2, caspase-3, tumor necrosis factor-alpha (TNF-α), and interleukin-1 (IL-1), were also noted, along with a decrease in HO-1 expression. Arsenic exposure led to a reduction in ovarian follicles and an increase in atretic follicles and uterine thickness. However, metformin significantly reduced ROS and MDA levels, enhanced antioxidant capacity, and protected ovarian tissue by upregulating heme oxygenase-1 (HO-1) and Bcl-2, modulating apoptotic and inflammatory genes, and preserving AMH levels. The possible protective role of metformin against arsenic-induced toxicity and its detrimental effects aims to improve therapeutic approaches to alleviate the harmful consequences of environmental pollutants, especially arsenic.