This review explores the hepatoprotective effects of flavonoids against benzo[a]pyrene (B[a]P)-induced oxidative liver damage through its metabolic pathways. B[a]P, a highly carcinogenic polycyclic aromatic hydrocarbon, is metabolized in the liver via enzymes such as CYP1A1 and CYP1B1, leading to the formation of reactive intermediates like BPDE, which cause DNA damage and oxidative stress. Flavonoids, natural compounds with antioxidant properties, can neutralize free radicals and mitigate oxidative stress. While extensive research has focused on the antioxidant effects of flavonoids, their role in regulating B[a]P metabolism to reduce oxidative stress remains underexplored. This review aims to summarize current knowledge on B[a]P-induced liver oxidative stress and the potential of flavonoids in mitigating its toxicity. B[a]P induces oxidative stress through the generation of reactive oxygen species (ROS), leading to DNA damage, mitochondrial dysfunction, and liver injury. Flavonoids counteract this by scavenging ROS, regulating antioxidant enzymes such as Nrf2, and modulating phase I, II, and III enzymes involved in xenobiotic metabolism. They enhance the detoxification of B[a]P metabolites, including BPDE, and reduce liver toxicity. Studies show that flavonoids like quercetin, kaempferol, and isorhamnetin influence B[a]P metabolism through different mechanisms, either accelerating or decelerating its detoxification. Additionally, flavonoids such as curcumin, isoorientin, and xanthohumol exhibit protective effects against B[a]P-induced liver damage by reducing oxidative stress, inflammation, and cell death. The review highlights the potential of flavonoids as natural hepatoprotective agents against B[a]P-induced liver diseases. Their ability to regulate B[a]P metabolism, reduce ROS production, and protect liver cells makes them promising candidates for therapeutic interventions. Further research is needed to fully understand the mechanisms by which flavonoids mitigate B[a]P toxicity and to develop effective strategies for liver protection.This review explores the hepatoprotective effects of flavonoids against benzo[a]pyrene (B[a]P)-induced oxidative liver damage through its metabolic pathways. B[a]P, a highly carcinogenic polycyclic aromatic hydrocarbon, is metabolized in the liver via enzymes such as CYP1A1 and CYP1B1, leading to the formation of reactive intermediates like BPDE, which cause DNA damage and oxidative stress. Flavonoids, natural compounds with antioxidant properties, can neutralize free radicals and mitigate oxidative stress. While extensive research has focused on the antioxidant effects of flavonoids, their role in regulating B[a]P metabolism to reduce oxidative stress remains underexplored. This review aims to summarize current knowledge on B[a]P-induced liver oxidative stress and the potential of flavonoids in mitigating its toxicity. B[a]P induces oxidative stress through the generation of reactive oxygen species (ROS), leading to DNA damage, mitochondrial dysfunction, and liver injury. Flavonoids counteract this by scavenging ROS, regulating antioxidant enzymes such as Nrf2, and modulating phase I, II, and III enzymes involved in xenobiotic metabolism. They enhance the detoxification of B[a]P metabolites, including BPDE, and reduce liver toxicity. Studies show that flavonoids like quercetin, kaempferol, and isorhamnetin influence B[a]P metabolism through different mechanisms, either accelerating or decelerating its detoxification. Additionally, flavonoids such as curcumin, isoorientin, and xanthohumol exhibit protective effects against B[a]P-induced liver damage by reducing oxidative stress, inflammation, and cell death. The review highlights the potential of flavonoids as natural hepatoprotective agents against B[a]P-induced liver diseases. Their ability to regulate B[a]P metabolism, reduce ROS production, and protect liver cells makes them promising candidates for therapeutic interventions. Further research is needed to fully understand the mechanisms by which flavonoids mitigate B[a]P toxicity and to develop effective strategies for liver protection.