One of the major public health issues is the rising prevalence of cataracts, a primary reason for preventable blindness. The causes for the development of age-related cataracts and accelerated cataractogenesis in diabetes are multifactorial. Hence, this study was designed to examine the status and relationship between the three majorly associated molecular events, namely, oxidative stress, non-enzymatic glycation, and polyol pathway in age-related cataracts with and without diabetes. A total of 472 subjects were distributed into four groups: non-diabetic subjects with clear lens (135), diabetic subjects with clear lens (40), non-diabetic subjects with cataract (174), and diabetic subjects with cataract (123). Cataracts were graded by slit-lamp examination according to the Lens Opacities Classification System III. Age at onset of cataract, type of opacity, anthropometric measurements, and sociodemographic characteristics were recorded, and clinical profile was examined. Plasma oxidative stress markers were assessed by estimating the lipid peroxidation end product malondialdehyde, protein oxidation products protein carbonyls, and DNA oxidative damage marker 8-hydroxy-2-deoxyguanosine. Plasma advanced glycation end products index, erythrocyte aldose reductase activity, and sorbitol levels were evaluated. After adjusting for age, plasma malondialdehyde levels were significantly higher in diabetic cataracts (P < 0.001) and non-diabetic cataract subjects (P < 0.05), compared to non-diabetic subjects with clear lens. Plasma advanced glycation end products index was significantly higher (P < 0.05) only in diabetic cataracts, but not in non-diabetic subjects with cataracts. Aldose reductase activity and sorbitol levels were significantly higher (P < 0.001) in both diabetic and non-diabetic subjects with cataract compared to non-diabetic subjects with clear lens. The data indicated that plasma lipid peroxidation in age-related cataracts was independent of diabetes. An association of pronounced glycation was observed only in diabetic cataracts but not in non-diabetic cataracts and polyol flux between diabetic cataracts and non-diabetic cataracts was comparable.

主要的公共卫生问题之一是白内障患病率上升，这是可预防的失明的主要原因。糖尿病中与年龄有关的白内障发展和白内障加速发展的原因是多方面的。因此，本研究旨在检查患有和不患有糖尿病的年龄相关性白内障中三个主要相关分子事件（氧化应激，非酶糖基化和多元醇途径）之间的状态和关系。总共472位受试者被分为四组：具有透明晶状体的非糖尿病受试者（135），具有透明晶状体的糖尿病受试者（40），患有白内障的非糖尿病受试者（174）和患有白内障的糖尿病受试者（123）。根据透镜不透明度分类系统III，通过裂隙灯检查对白内障进行分级。白内障发病年龄，记录不透明类型，人体测量学和社会人口统计学特征，并检查临床资料。通过估计脂质过氧化终产物丙二醛，蛋白氧化产物蛋白羰基和DNA氧化损伤标记物8-羟基-2-脱氧鸟苷来评估血浆氧化应激标记物。评估血浆高级糖基化终产物指数，红细胞醛糖还原酶活性和山梨醇水平。调整年龄后，糖尿病性白内障患者血浆丙二醛水平明显升高（和DNA氧化损伤标记物8-羟基-2-脱氧鸟苷。评估血浆高级糖基化终产物指数，红细胞醛糖还原酶活性和山梨醇水平。调整年龄后，糖尿病性白内障患者血浆丙二醛水平明显升高（和DNA氧化损伤标记物8-羟基-2-脱氧鸟苷。评估血浆晚期糖基化终产物指数，红细胞醛糖还原酶活性和山梨糖醇水平。调整年龄后，糖尿病性白内障患者血浆丙二醛水平明显升高（P  <0.001）和非糖尿病性白内障患者（P  <0.05），与非透明性晶状体糖尿病患者相比。 仅在糖尿病性白内障中，血浆晚期糖基化终末产物指数显着较高（P <0.05），而在非糖尿病性白内障中则没有。醛糖还原酶活性和山梨糖醇水平显着较高（P 与具有透明晶状体的非糖尿病受试者相比，患有白内障的糖尿病和非糖尿病受试者均<0.001）。数据表明与年龄有关的白内障中血浆脂质过氧化与糖尿病无关。仅在糖尿病性白内障中观察到明显糖基化的关联，而在非糖尿病性白内障中则未观察到，并且糖尿病性白内障和非糖尿病性白内障之间的多元醇通量相当。