Marques Luiza S, Zborowski Vanessa A, Heck Suélen O, Fulco Bruna C W, Nogueira Cristina W
Laboratory of Synthesis, Reactivity, Pharmacological and Toxicological Evaluation of Organochalcogens, Department of Biochemistry and Molecular Biology, Center of Natural and Exact Sciences, Federal University of Santa Maria, Santa Maria, RS 97105-900, Brazil.
Departamento de Bioquímica e Biologia Molecular, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, Santa Maria, CEP 97105-900, RS, Brazil.
Can J Physiol Pharmacol. 2021 Sep;99(9):943-951. doi: 10.1139/cjpp-2020-0652. Epub 2021 Apr 16.
Streptozotocin (STZ) is a substance used experimentally to induce a diabetes model, a metabolic disease associated with oxidative tissue damage. This study evaluated if 4-4'-dichloro-diphenyl diselenide (-ClPhSe) modulates oxidative stress in peripheral tissues of diabetic mice. Male Swiss mice received a single STZ injection (i.p.) at a dose of 200 mg/kg or its vehicle and were treated with (-ClPhSe) (7 days, 5 mg/kg) or metformin (200 mg/kg, twice per day). After, the mice were euthanized to collect liver, kidney, and skeletal muscle samples. In the liver, (-ClPhSe) reduced thiobarbituric acid reactive substances (TBARS) and protein carbonyl levels and normalized the superoxide dismutase activity in STZ-treated mice. In the kidney, (-ClPhSe) reversed the increase in the reactive species levels but not the catalase (CAT) activity reduction in STZ-treated mice. There was no evidence of oxidative damage in the skeletal muscle of STZ-treated mice, but an increase in the CAT activity and a reduction in non-protein thiol levels were found. (-ClPhSe) did not reverse a decrease in hepatic and renal δ-aminolevulinic acid dehydratase activity in STZ-treated mice. The results show that the liver and kidney of STZ-treated mice were more susceptible to oxidative stress. This study reveals that (-ClPhSe) modulated oxidative stress, which differently affected peripheral tissues of diabetic mice.
链脲佐菌素（STZ）是一种用于实验诱导糖尿病模型的物质，糖尿病是一种与氧化组织损伤相关的代谢性疾病。本研究评估了4-4'-二氯二苯二硒醚（-ClPhSe）是否能调节糖尿病小鼠外周组织中的氧化应激。雄性瑞士小鼠接受一次腹腔注射剂量为200 mg/kg的STZ或其溶媒，并分别用（-ClPhSe）（7天，5 mg/kg）或二甲双胍（200 mg/kg，每天两次）进行处理。之后，对小鼠实施安乐死以采集肝脏、肾脏和骨骼肌样本。在肝脏中，（-ClPhSe）降低了硫代巴比妥酸反应性物质（TBARS）和蛋白质羰基水平，并使STZ处理小鼠的超氧化物歧化酶活性恢复正常。在肾脏中，（-ClPhSe）逆转了STZ处理小鼠中活性物质水平的升高，但未逆转过氧化氢酶（CAT）活性的降低。在STZ处理小鼠的骨骼肌中没有氧化损伤的证据，但发现CAT活性增加且非蛋白巯基水平降低。（-ClPhSe）未能逆转STZ处理小鼠肝脏和肾脏中δ-氨基乙酰丙酸脱水酶活性的降低。结果表明，STZ处理小鼠的肝脏和肾脏对氧化应激更敏感。本研究表明，（-ClPhSe）可调节氧化应激，且对糖尿病小鼠外周组织的影响存在差异。
