BACKGROUND Erythrocytes of diabetic cats have decreased superoxide dismutase activity, possibly indicative of oxidative stress. HYPOTHESIS Erythrocytes of diabetic cats undergo oxidative stress, which is caused by hyperglycemia and hyperlipidemia, and improves with treatment. ANIMALS Twenty-seven client-owned cats with diabetes mellitus, 11 matched healthy cats, and 21 purpose-bred healthy cats. METHODS Prospective study. Advanced oxidized protein products, carbonyls (protein oxidation by-products), and thiols (antioxidants) were quantified in erythrocyte membrane, thiobarbituric acid reactive substances (TBAR, lipid peroxidation by-products), and thiols in erythrocyte cytoplasm of all cats. Comparison were performed between diabetic and matched healthy cats, between diabetic cats achieving remission or not, and among purpose-bred cats after 10 days of hyperglycemia (n = 5) or hyperlipidemia (n = 6) versus controls treated with saline (n = 5) or untreated (n = 5). RESULTS Compared with controls, erythrocytes of diabetic cats initially had higher median membrane carbonyls (4.6 nmol/mg total protein [range: 0.1-37.7] versus 0.7 [0.1-4.7], P < .001) and lower cytoplasmic TBAR (1.9 nmol/mg [0.5-2.4] versus 2.4 [1.4-3.5] P < .001), and thiols (419 nmol/mg [165-621] versus 633 [353-824], P < 0.001). After 12-16 weeks of treatment in diabetic cats, carbonyls decreased by 13% (P < .001), but remained higher (P < .001) and TBAR and thiols lower (P = .02, P < .001) than those in controls. No differences were observed between diabetic cats achieving remission or not, and among purpose-bred cats. CONCLUSIONS AND CLINICAL IMPORTANCE Diabetes mellitus is associated with increased protein oxidation and reduced antioxidant defenses, which persist during treatment and remission, although mild improvement in protein oxidation occurs. Short-term hyperglycemia or hyperlipidemia does not cause oxidative stress. The reason for decreased TBAR remains unknown.

中文翻译：

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糖尿病猫的红细胞，高血糖和高血脂的氧化状态。

背景技术糖尿病猫的红细胞具有降低的超氧化物歧化酶活性，这可能表明氧化应激。假设糖尿病猫的红细胞受到氧化应激，这是由高血糖和高血脂引起的，并随着治疗而改善。动物27只患有糖尿病的客户拥有的猫，11只匹配的健康猫和21只专用健康猫。方法前瞻性研究。对所有猫的红细胞膜，硫代巴比妥酸反应性物质（TBAR，脂质过氧化副产物）和巯基中的高级氧化蛋白产物，羰基（蛋白氧化副产物）和硫醇（抗氧化剂）进行了定量。比较了糖尿病猫和配对的健康猫，是否达到缓解状态的糖尿病猫，在高血糖（n = 5）或高脂血症（n = 6）10天后的目的猫中，与生理盐水（n = 5）或未治疗（n = 5）的对照相比。结果与对照组相比，糖尿病猫的红细胞最初具有更高的中位膜羰基羰基含量（4.6 nmol / mg总蛋白[范围：0.1-37.7]对0.7 [0.1-4.7]，P <.001）和较低的胞质TBAR（1.9 nmol / mg）。毫克[0.5-2.4]对比2.4 [1.4-3.5] P <.001）和硫醇（419 nmol /毫克[165-621]对比633 [353-824]，P <0.001）。在糖尿病猫中治疗12-16周后，羰基比那些降低了13％（P <.001），但仍然更高（P <.001），TBAR和硫醇更低（P = .02，P <.001）在控件中。在未达到缓解或未达到缓解的糖尿病猫之间以及目的型猫之间未观察到差异。结论和临床意义糖尿病与蛋白质氧化增加和抗氧化防御能力降低有关，尽管在蛋白质氧化中会出现轻度改善，但糖尿病在治疗和缓解期间仍会持续存在。短期高血糖症或高血脂症不会引起氧化应激。TBAR降低的原因仍然未知。