Life Sciences 2019-Aug
Dietary inorganic nitrate attenuates hyperoxia-induced oxidative stress in obese type 2 diabetic male rats.
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Abstrakts
MAIN METHODS
Fifty-six male Wistar rats (190-210 g) were divided into 8 groups: Controls (non-treated, nitrate-treated, O2-treated, and nitrate + O2-treated) and diabetes (non-treated, nitrate-treated, O2-treated, and nitrate + O2-treated). Diabetes was induced using high-fat diet and low-dose of streptozotocin (30 mg/kg). Rats in intervention groups, were exposed to 95% oxygen and consumed sodium nitrate (100 mg/L) in drinking water. Serum fasting glucose, oxidized (GSSG) and reduced (GSH) glutathiones, total oxidant status (TOS), catalase and superoxide dismutase (SOD) activities, and total antioxidant capacity (TAC) were measured after intervention. Oxidative stress index (OSI) was calculated as TOS/TAC ratio.KEY FINDINGS
Diabetic rats had increased oxidative stress and hyperoxia exacerbated it. In O2-diabetic rats, nitrate decreased GSSG (102.7 ± 2.1 vs. 236.0 ± 20.1 μM, P < 0.001), TOS (67.7 ± 7.3 vs. 104 ± 3.8 μM, P < 0.001), and OSI (0.44 ± 0.04 vs. 0.91 ± 0.07, P < 0.001) and increased catalase (2.8 ± 0.13 vs. 1.8 ± 0.21 KU/L, P = 0.014), SOD (53.4 ± 1.5 vs. 38.4 ± 1.2 U/mL, P < 0.001), GSH (43.7 ± 1.4 vs. 17.8 ± 0.5 mM, P = 0.003), TAC (152.5 ± 1.9 vs. 116.7 ± 5.0 mM, P < 0.001), and GSH/GSSG ratio (0.43 ± 0.01 vs. 0.08 ± 0.01, P = 0.005). Nitrate also potentiated effects of hyperoxia on decreasing fasting glucose.