OBJECTIVES: This study was focused on the monitoring how the anti-inflammatory substance, N(1)-methylnicotinamide (MNA), could influence oxidation and glycooxidation stress markers in rats under conditions of streptozotocin (STZ)-induced diabetes mellitus. METHODS: Diabetes mellitus was induced in 60 male Wistar rats by intraperitoneal injection of STZ and after 7 days diabetic animals were allocated to five groups according to the dose of MNA administered for 7 weeks. The degree of DNA damage in lymphocytes, as well as advanced glycation endproducts (AGEs), protein carbonyls, lipid peroxides, and total antioxidant capacity (TEAC) in plasma were measured. RESULTS: Glycation damage to proteins (represented by AGEs level) was significantly increased in all diabetic groups compared to untreated non-diabetic animals. MNA did not affect TEAC of plasma in any group of diabetic rats. Supplementation of diabetic rats with MNA at the dose of 200 mg/kg resulted in decreased protein carbonyls (from 0.0818±0.0091 to 0.0558±0.0044 nmol/mg proteins; P<0.05, n=15) and DNA oxidation, reflected by the levels of 8-oxoG (0.6302±0.085 vs. 0.9213±0.108 8-oxoG/10(6) G; P<0.05, n=15), compared to untreated diabetic animals. DISCUSSION: Our results demonstrated that MNA at suitable concentrations could influence oxidative modifications of proteins and DNA.
OBJECTIVES: This study was focused on the monitoring how the anti-inflammatory substance, N(1)-methylnicotinamide (MNA), could influence oxidation and glycooxidation stress markers in rats under conditions of streptozotocin (STZ)-induced diabetes mellitus. METHODS:Diabetes mellitus was induced in 60 male Wistar rats by intraperitoneal injection of STZ and after 7 days diabetic animals were allocated to five groups according to the dose of MNA administered for 7 weeks. The degree of DNA damage in lymphocytes, as well as advanced glycation endproducts (AGEs), protein carbonyls, lipid peroxides, and total antioxidant capacity (TEAC) in plasma were measured. RESULTS: Glycation damage to proteins (represented by AGEs level) was significantly increased in all diabetic groups compared to untreated non-diabetic animals. MNA did not affect TEAC of plasma in any group of diabeticrats. Supplementation of diabeticrats with MNA at the dose of 200 mg/kg resulted in decreased protein carbonyls (from 0.0818±0.0091 to 0.0558±0.0044 nmol/mg proteins; P<0.05, n=15) and DNA oxidation, reflected by the levels of 8-oxoG (0.6302±0.085 vs. 0.9213±0.108 8-oxoG/10(6) G; P<0.05, n=15), compared to untreated diabetic animals. DISCUSSION: Our results demonstrated that MNA at suitable concentrations could influence oxidative modifications of proteins and DNA.
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