Departments of Biochemistry& Statistics, National Institute of Nutrition, Hyderabad, India.
Anand Eye Institute, Habsiguda, India.
Exp Eye Res. 2020 Nov;200:108230. doi: 10.1016/j.exer.2020.108230. Epub 2020 Sep 12.
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.
一个主要的公共卫生问题是白内障的患病率上升，这是可预防失明的主要原因。年龄相关性白内障和糖尿病加速白内障形成的原因是多因素的。因此，本研究旨在检查与年龄相关的白内障和糖尿病相关白内障中三种主要相关分子事件（即氧化应激、非酶糖基化和多元醇途径）的状态和关系。共有 472 名受试者分为四组：无糖尿病的透明晶状体受试者（135 名）、有糖尿病的透明晶状体受试者（40 名）、无糖尿病的白内障受试者（174 名）和有糖尿病的白内障受试者（123 名）。白内障根据 Lens Opacities Classification System III 通过裂隙灯检查进行分级。记录白内障发病年龄、混浊类型、人体测量学测量值和社会人口学特征，并进行临床检查。通过评估脂质过氧化终产物丙二醛、蛋白质氧化产物蛋白羰基和 DNA 氧化损伤标志物 8-羟基-2-脱氧鸟苷来评估血浆氧化应激标志物。评估了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醇水平。调整年龄后，糖尿病性白内障（P < 0.001）和非糖尿病性白内障受试者（P < 0.05）的血浆丙二醛水平明显高于无糖尿病的透明晶状体受试者。仅在糖尿病性白内障中，血浆晚期糖基化终产物指数显著升高（P < 0.05），而非糖尿病性白内障受试者中则无此现象。与无糖尿病的透明晶状体受试者相比，糖尿病和非糖尿病白内障受试者的醛糖还原酶活性和山梨醇水平均显著升高（P < 0.001）。数据表明，年龄相关性白内障中的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的糖化作用，而非糖尿病性白内障中则无此现象，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。
