Pulmonary Protective Effects of Vitamin D and N-acetylcysteine on Paraquat-induced Lung Toxicity in Rats: Modulation of Oxidant / Antioxidant Balance

Background: Paraquat (PQ) is one of the most common herbicides used in agriculture that can lead to very acute toxicity in mammals. It has been reported that PQ has destructive effects on the lungs. Objective: We aimed to investigate the effect of N-acetyl Cysteine (NAC) and Vitamin D (Vit D) on the oxidative toxicity of the lung in subacute paraquat exposure. 36 male albino Wistar rats at 8 weeks were randomly divided into 6 groups (n=6). A control group, a PQ-intoxicated group (5 mg/kg body weight), a Vit D-treated group (2 μg/kg), an NAC-treated group, a PQ (6.25 mg/kg) + Vit D group, and finally a PQ + NAC group, each was treated for 7 days. Methods: In this experimental study, Lipid Peroxidation (LPO), Total Oxidant Status (TOS), Total Antioxidant Capacity (TAC), Total Thiol Groups (TTG), and Hydroxyproline (Hyp) levels in lung tissue were evaluated. Results: PQ exposure resulted in a substantial elevation of LPO, TOS, and Hyp levels. Conversely, TAC and TTG content demonstrably declined. Administration of either PQ+Vit D or PQ+NAC significantly reduced LPO, TOS, and Hyp levels in the PQ-exposed rats compared to the PQ group alone. Conversely, TAC and TTG content significantly increased in these groups. These findings suggest that both vitamin D and NAC may function as free radical scavengers and potential antioxidant agents, potentially alleviating the detrimental effects of PQ poisoning on the lungs. Conclusion: The present study has demonstrated the administration of Vit D and NAC to significantly mitigate PQ-induced lung injury in rats. This protective effect can be likely attributed to their modulation of the oxidant/antioxidant balance, as evidenced by reductions in LPO, TOS, and Hyp levels, alongside increases in TAC and TTG content. These findings suggest that vitamin D and NAC may function as free radical scavengers and antioxidant enhancers, offering protection against PQ-induced oxidative stress and subsequent lung tissue damage.