Clinic for Small Animal Internal Medicine, Vetsuisse Faculty, University of Zurich, Zurich, Switzerland.
Department of Animal Medicine, Production and Health, University of Padova, Padua, Italy.
J Vet Intern Med. 2020 Mar;34(2):616-625. doi: 10.1111/jvim.15732. Epub 2020 Feb 16.
Erythrocytes of diabetic cats have decreased superoxide dismutase activity, possibly indicative of oxidative stress.
Erythrocytes of diabetic cats undergo oxidative stress, which is caused by hyperglycemia and hyperlipidemia, and improves with treatment.
Twenty-seven client-owned cats with diabetes mellitus, 11 matched healthy cats, and 21 purpose-bred healthy cats.
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).
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.
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.
糖尿病猫的红细胞中超氧化物歧化酶活性降低，这可能表明存在氧化应激。
糖尿病猫的红细胞发生氧化应激，这是由高血糖和高血脂引起的，并且随着治疗而改善。
27 只患有糖尿病的患宠猫、11 只匹配的健康猫和 21 只目的培育的健康猫。
前瞻性研究。定量测定所有猫的红细胞膜中的高级氧化蛋白产物（蛋白质氧化产物）、羰基（蛋白氧化副产物）和巯基（抗氧化剂），红细胞细胞质中的硫代巴比妥酸反应物质（TBAR，脂质过氧化副产物）和巯基。将糖尿病猫与匹配的健康猫进行比较，将缓解和未缓解的糖尿病猫进行比较，并将接受高血糖（n = 5）或高血脂（n = 6）治疗 10 天后的目的培育猫与接受生理盐水（n = 5）或未治疗（n = 5）的对照猫进行比较。
与对照组相比，糖尿病猫的红细胞膜初始时的羰基中位数较高（4.6 nmol/mg 总蛋白[范围：0.1-37.7] 比 0.7[0.1-4.7]，P <0.001），细胞质中的 TBAR 较低（1.9 nmol/mg[0.5-2.4] 比 2.4[1.4-3.5]，P <0.001），巯基较低（419 nmol/mg[165-621] 比 633[353-824]，P <0.001）。在糖尿病猫接受 12-16 周治疗后，羰基降低了 13%（P <0.001），但仍高于对照组（P <0.001），TBAR 和巯基仍较低（P =0.02，P <0.001）。未缓解的糖尿病猫之间或目的培育的猫之间没有差异。
糖尿病与蛋白质氧化增加和抗氧化防御降低有关，尽管蛋白质氧化有轻微改善，但这种情况在治疗和缓解期间仍然存在。短期高血糖或高血脂不会引起氧化应激。TBAR 减少的原因尚不清楚。
