Cheng H M
Howe Laboratory of Ophthalmology, Harvard Medical School, Boston, Mass. 02114.
Metab Pediatr Syst Ophthalmol (1985). 1988;11(4):152-5.
Rat lenses treated with greater than 0.06 mM hydrogen peroxide (HP) appeared to sustain epithelial damage, particularly a loss of enzymes including hexokinase, which controls the supply of glucose-6-phosphate. This may account for the lower level of hexose monophosphate shunt activation observed in these lenses. Other alterations include a decrease of lactate production and disturbance to ionic balance. These changes occurred despite HP removal by glutathione reductase/peroxidase system, catalase and other mechanisms. This suggests an inherent weakness for the lens to resist stresses from high levels of HP. Further, competition for NADPH between aldose reductase and glutathione reductase apparently affects the lens's ability to detoxify HP. This implies a role for oxidation in diabetic cataractogenesis.
用大于0.06 mM过氧化氢（HP）处理的大鼠晶状体似乎遭受了上皮损伤，尤其是包括己糖激酶在内的多种酶的丧失，己糖激酶控制着6-磷酸葡萄糖的供应。这可能解释了在这些晶状体中观察到的磷酸戊糖途径激活水平较低的原因。其他变化包括乳酸生成减少和离子平衡紊乱。尽管通过谷胱甘肽还原酶/过氧化物酶系统、过氧化氢酶和其他机制去除了HP，但这些变化仍会发生。这表明晶状体在抵抗高水平HP应激方面存在内在弱点。此外，醛糖还原酶和谷胱甘肽还原酶之间对NADPH的竞争显然会影响晶状体对HP解毒的能力。这意味着氧化在糖尿病性白内障形成中起作用。
