<p>The widespread incidence of brain tumors presents a substantial obstacle to public health due to their debilitating and lethal outcomes. Although the etiology of brain tumors is still an enigma, emerging evidence indicates a strong correlation between pesticide exposure and the onset of brain cancer. The commonly used pesticides, including organophosphates, organochlorines and pyrethroids, exert their toxic effects by inducing oxidative stress that causes damage to nucleic acids, lipids, and proteins. Oxidative stress is a significant factor in the development of brain cancer mainly due to its elevated oxygen consumption and abundance of polyunsaturated fatty acids that make it more susceptible to oxidative harm. Pesticides induce oxidative stress through various pathways, such as JAK-STAT and Keap1/Nrf2/ARE, which regulate reactive oxygen species production and antioxidant responses. Despite extensive research linking pesticides to brain tumors, precise molecular mechanisms remain unclear. The present review attempts to discuss the molecular mechanisms by which pesticides induce oxidative stress and explores the interplay between various signaling pathways in regulating reactive oxygen species and reactive nitrogen species. It also highlights the complicated relationship between pesticide-induced oxidative stress and brain cancer development and emphasizes the need for further investigation into the genetic and epigenetic impacts of pesticides on xenobiotic detoxification systems and the production of oncometabolites. By providing a comprehensive overview of the molecular foundations of pesticide-mediated genetic damage, this paper aims to contribute significantly to the existing literature for developing regulatory measures and safer alternatives to mitigate the health risks associated with pesticide exposure.</p> Graphical Abstract <p></p>