PurposeTo evaluate modes of cataractogenesis in the hypertensive state by using different hypertensive animal models, including fructose, cadmium chloride (CdCl2), Nω-nitro-l-arginine methyl ester (l-NAME), and two-kidney, one clip (2K1C) method.MethodsMale Sprague–Dawley albino rats (150–180 g) were divided into different groups, each group containing six animals. Hypertension was induced in animals via six weeks administration of fructose (10% solution in drinking water), CdCl2 (0.5 mg/kg/day, i.p.), and l-NAME (20 mg/kg/day, p.o.) in their respective groups and NaCl (0.9% solution in drinking water) in the 2K1C group. The Ramipril-treated group (2 mg/kg/day, orally) served as a standard group for the 2K1C animal model. Blood pressure was measured biweekly using non-invasive blood pressure system. The biochemical parameters in serum and eye lenses were evaluated after six weeks of the experimental protocol.ResultsHypertensive animal models showed significant induction of systolic and diastolic blood pressure and modulation of oxidative stress through depletion of antioxidants, including glutathione peroxidase, catalase, superoxide dismutase, glutathione, and elevation of malondialdehyde in serum and eye lenses. A significant elevation of ionic contents (Na+ and Ca2+) and reduction of total protein and Ca2+ ATPase activity in eye lenses were observed in all hypertensive animal models except l-NAME when compared with the normal group. The significant restoration of the antioxidants, Malondialdehyde (MDA) total protein, and ionic contents in the eye lenses concomitant with reduction of blood pressure were observed in the ramipril-treated group as compared to the 2K1C animal model. The results indicate that the fructose, CdCl2, and 2K1C models showed pronounced cataractogenic effects in the rat eye lenses.ConclusionBased on our findings, it can be concluded that systemic hypertension significantly increases the risk of cataract formation in the rat eyes via modulation of the antioxidant defense mechanism and electrolyte homeostasis.

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Objectives:Several studies have revealed that systemic hypertension is strongly associated with cataractogenesis. However, the pathophysiology and treatment is often unclear. In this study, we evaluated the anti-cataractogenic effect of cinnamaldehyde (CA), a natural organic compound, in rats with fructose-induced hypertension.Methods:The rats were divided into six groups. For six weeks, the normal group received a suspension of 0.5% carboxy methyl cellulose (10 mL/kg/day, p.o.) while five other groups received a 10% (w/v) fructose solution in their drinking water to induce hypertension. By the end of the third week hypertension had been induced in all the animals receiving fructose. From the beginning of the fourth week to the end of the sixth week, one of those five groups (control) continued to receive only 10% (w/v) fructose solution, one group (standard) received ramipril (1 mg/kg/day, p.o.) plus 10% (w/v) fructose solution, and three groups (experimental) received CA at doses of 20, 30, and 40 mg/kg/day p.o., plus 10% (w/v) fructose solution. Blood pressure was measured weekly using a non-invasive blood pressure apparatus. After six weeks, the animals were sacrificed, and the anti-cataractogenic effects on the eye lenses were evaluated.Results:Administration of fructose elevated both the systolic and the diastolic blood pressures, which were significantly reduced by CA at all dose levels. In the control group, a significant increase in the malonaldehyde (MDA) level and decreases in the total protein, Ca2+adenosine triphosphate (ATP)ase activity, glutathione peroxidase, catalase, superoxide dismutase and glutathione levels, as compared to the normal group, were observed. Administration of CA at all doses significantly restored the enzymatic, non-enzymatic, antioxidants, total protein, and Ca2+ATPase levels, but decreased the MDA level, as compared to the control group.Conclusion:The present study revealed that CA modulated the antioxidant parameters of the serum and lens homogenates in hypertension-induced cataractogenic animals.