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The toxicity and related mechanisms of aflatoxin B1 (AFB1) and aflatoxin M1 (AFM1) in the mouse kidney were studied, and the role of <span style="font-variant: small-caps;">l</span>-proline in alleviating kidney damage was investigated. In a 28-day toxicity mouse model, thirty mice were divided into six groups: control (without treatment), <span style="font-variant: small-caps;">l</span>-proline group (10 g/kg body weight (b.w.)), AFB1 group (0.5 mg/kg b.w.), AFM1 (3.5 mg/kg b.w.), AFB1 + <span style="font-variant: small-caps;">l</span>-proline group and AFM1 + <span style="font-variant: small-caps;">l</span>-proline group. Kidney index and biochemical indicators were detected, and pathological staining was observed. Using a human embryonic kidney 293 (HEK 293) cell model, cell apoptosis rate and apoptotic proteins expressions were detected. The results showed that AFB1 and AFM1 activated pathways related with oxidative stress and caused kidney injury; <span style="font-variant: small-caps;">l</span>-proline significantly alleviated abnormal expressions of biochemical parameters and pathological kidney damage, as well as excessive cell apoptosis in the AF-treated models. Moreover, proline dehydrogenase (PRODH) was verified to regulate the levels of <span style="font-variant: small-caps;">l</span>-proline and downstream apoptotic factors (Bax, Bcl-2, and cleaved Caspase-3) compared with the control (<i>p</i> &lt; 0.05). In conclusion, <span style="font-variant: small-caps;">l</span>-proline could protect mouse kidneys from AFB1 and AFM1 through alleviating oxidative damage and decreasing downstream apoptosis, which deserves further research and development.