Abstract
Background: Erythrocytes of diabetic cats have decreased superoxide dismutaseactivity, possibly indicative of oxidative stress.
Hypothesis: Erythrocytes of diabetic cats undergo oxidative stress, which is causedby hyperglycemia and hyperlipidemia, and improves with treatment.
Animals: Twenty-seven client-owned cats with diabetes mellitus, 11 matched healthycats, and 21 purpose-bred healthy cats.
Methods: Prospective study. Advanced oxidized protein products, carbonyls (proteinoxidation by-products), and thiols (antioxidants) were quantified in erythrocyte mem-brane, thiobarbituric acid reactive substances (TBAR, lipid peroxidation by-products),and thiols in erythrocyte cytoplasm of all cats. Comparison were performed betweendiabetic and matched healthy cats, between diabetic cats achieving remission or not,and among purpose-bred cats after 10 days of hyperglycemia (n = 5) or hyperlipid-emia (n = 6) versus controls treated with saline (n = 5) or untreated (n = 5).
Results: Compared with controls, erythrocytes of diabetic cats initially had highermedian 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 by13% (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 catsachieving remission or not, and among purpose-bred cats.
Conclusions and Clinical Importance:Diabetes mellitus is associated with increasedprotein oxidation and reduced antioxidant defenses, which persist during treatment and remission, although mild improvement in protein oxidation occurs. Short-termhyperglycemia or hyperlipidemia does not cause oxidative stress. The reason fordecreased TBAR remains unknown.
Zini, Eric