Introduction: The lung is the primary organ for inhaled irritants. Chlorine (Cl2) has high solubility in water. It can dissolve into epithelial lining fluid when contacting mucosal surfaces. Vitamin C provided an important antioxidant defense against hypochlorous acid-mediated injury in atherosclerosis. Vitamin C supplementation decreased lipid and protein oxidation in vivo.
Aim: To study the possible protective role of Vitamin C against the toxic effects of Cl2 on the lung of adult albino rats with special emphasis on the vascular endothelial growth factor (VEGF).
Materials and Methods: Forty male rats were divided into four equal groups. Group (A) control rats, group (B) rats received Vitamin C (500 mg/kg) orally once per day for 8 weeks, group (C) rats were exposed to Cl2 for 4 h daily for of 8 weeks and group (D) Cl2-Vitamin C group received Vitamin C and exposed to Cl2 as in group B and C. At the end of the experiment lungs were prepared and stained with H&E, Masson's trichrome and immunohistological stain for VEGF.
Results: Examination of specimens of group C showed marked loss of normal architecture. The lung showed widen alveoli containing vacuolated acidophilic exudate entangled with polymorph nuclear leucocytes. The wall of the bronchioles showed vacuolated acidophilic exudate. Lung specimens stained by Masson's trichrome stain showed increased collagen deposition around the bronchioles and the blood vessels. Also this group showed strong positive reaction to vascular endothelial growth factor (VEGF). Group D showed improved lung architecture and VEGF moderate reaction.
Conclusion: Cl2 has destructive changes in the architecture of the lung. In addition, it creates a case similar to hypoxia indicated by strong reaction to VEGF that has been ameliorated by vitamin C.