Background Age-related cataract is a common cause of blindness.However,its cause and pathogenic mechanism have not been fully understood.Recent studies revealed that aquaporin 1 (AQP1) and AQP0 are closely related to the pathogenesis of cataract.Objective This study was to investigate the differential distribution and expression of AQP0 and AQP1 in lenses with age-related cataract and explore its effect on pathogenesis of age-related cataract.Methods Seventeen anterior capsular membrane samples and nucleus samples of lenses were collected from age-related cataract patients during the small incision nonphacoemulsification cataract extraction,and 6 normal lens samples were obtained from health donors in the First Affiliated Hospital of Fujian Medical University.The expression and distribution of AQP1 and AQP0 in the lenses were detected by immunohistochemistry,and the relative expression levels of AQP1 and AQP0 proteins in the lenses were assayed by using Western blot assay.This study protocol was approved by Ethic Committee of this hospital,and written informed consent was obtained from each patient.Results Immunohistochemistry showed that in the normal lenses,AQP1 expressed mainly in LECs;while AQP0 primarily expressed in fiber cells of the lens cortex and nucleus.The relative expression levels of AQP1 and AQP0 in the lenses with age-related cataract (absorbance) were 0.223±0.008 and 0.118±0.015,which were significantly lower than 0.246±0.007 and 0.149±0.007 in the normal lenses (t =-4.508,-3.291,both at P＜0.01).Western blot revealed that the relative expression levels of AQP1 and AQP0 in the lenses with age-related cataract (absorbance) were 0.663 ± 0.012 and 0.599 ± 0.015,which were significantly reduced in comparison with 0.844±0.041 and 0.955 ±0.064 in the normal lenses (t =-7.492,P＜0.05;t =-9.570,P＜0.01).Conclusions AQP1 and AQP0 distribute in different sites of lenses.The expressions of AQP1 and AQP0 are obviously down-regulated in lenses with age-related cataract,suggesting that AQP1 and AQP0 probably play different roles in the pathogenesis of age-related cataract.