Protective effect of N-acetylcysteine (NAC) against Di-ethylhexyl phthalate (DEHP) induced pulmonary toxicity in male albino rats (histological and immunohistochemical study)

Document Type : Original Article

Authors

1 Department of Forensic Medicine and Clinical Toxicology, Faculty of Medicine, Banha University, Banha 13518, Egypt

2 Department of Histology and Cell Biology, Faculty of Medicine, Banha University, Banha 13518, Egypt

3 Department of Microbiology and Immunology, Faculty of Medicine, Banha University, Banha 13518, Egypt

4 Department of Pharmacology, Faculty of Medicine, Banha University, Banha 13518, Egypt

5 benha faculty of medicine

Abstract

Di-ethylhexyl phthalate (DEHP) is a global environmental pollutant. Human exposure to DEHP occurs through environmental sources. Community exposure (food, air, water) as well as medical settings’ exposure impose crucial effects on the human health. DEHP had been reported to have cytotoxic, immunotoxic, genotoxic, and reproductive toxic properties. This work aims to assess the possible toxic effects of DEHP on adult albino rats' lungs and to evaluate the possible protective effects of N-acetylcysteine (NAC) using body weight and relative lung weight parameters. Assessment of DHEP toxicity is measured by biochemical, histopathological and immunohistochemical methods. Fifty male adult albino rats were divided into five equal groups as follows: Group Ι (Negative control group), Group ΙΙ (Positive control group), Group IΙΙ (NAC-treated group): was given NAC orally (200 mg/kg/day), Group IV (DEHP-treated group): was given DEHP orally (3gm/kg once daily for 4 weeks) and Group V: (DEHP + NAC-treated group): was treated with DEHP concomitantly with NAC at the same previous doses. The results of the present study revealed that DEHP has significantly increased the lipid peroxidation level and significantly reduced glutathione content (GSH), superoxide dismutase (SOD) activity and catalase activity. The histological results of group IV showed inflammatory cellular infiltration of the lungs associated with interstitial edema, hemorrhage and inter-alveolar septal thickening that were markedly reduced in group V. Also, group V, showed a significant decrease in the collagen fibers accumulation and in caspase-3 expression as compared to group IV. Conclusion: treatment with NAC can protect against DEHP induced pulmonary toxicity in rats by decreasing oxidative stress, inflammation and apoptosis.

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