Role of Nitric Oxide in the Development of Cataract Formation in CdCl2-induced Hypertensive Animals

Abstract

ABSTRACT Purpose Previously we established a strong association of systemic hypertension with cataract formation. In the present study, we investigated the role of nitric oxide (NO) in the development of cataract formation in CdCl2-induced hypertensive animals. Materials and Methods Hypertension was induced in male albino rats by intraperitoneal administration of CdCl2 (0.5 mg/kg/day) for eight weeks. The NO modulators, 10 µM S-nitrosoglutathione (NO donor) and 1% w/v Nω-nitro-L-arginine methyl ester (L-NAME, NOS inhibitor) were applied topically once a day on the eye cornea during the experimental period. Amlodipine (3mg/kg/day) was used as a standard antihypertensive drug and administered orally. Results In the CdCl2 control group, mean arterial pressure was significantly increased along with augmentation of lens nitrite, opacity, and oxidative stress. The control of hypertension by amlodipine substantially restored lens nitrite and cataractogenic events. Moreover, topical application of L-NAME significantly alleviated the lens nitrite, opacity, antioxidants (GSH, CAT, SOD, and GPx), MDA, proteins, and ionic (Na+ and Ca2+) contents. Whereas, S-nitrosoglutathione topical application exacerbated these cataractogenic events without affecting hypertension as compared to CdCl2 control group. The findings demonstrated that NO donor exacerbates and NOS inhibitor alleviates the cataract formation in hypertensive condition. The control of hypertension also reduces the cataract formation with reduction of lens nitrite level. Conclusion The overall findings suggested the strong correlation between NO and hypertension associated cataract formation. The elevation of lens nitrite (NO metabolite) is one of the key factors of augmentation of lenticular oxidative stress and cataract formation in the hypertensive condition.