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被动吸烟会导致幼鼠大脑发生氧化损伤:二苯基二硒醚的保护作用。

Passive smoke exposure induces oxidative damage in brains of rat pups: Protective role of diphenyl diselenide.

作者信息

Stangherlin Eluza Curte, Luchese Cristiane, Ardais Ana Paula, Nogueira Cristina Wayne

机构信息

Departamento de Química, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, Brazil.

出版信息

Inhal Toxicol. 2009 Aug;21(10):868-74. doi: 10.1080/08958370802526881.

DOI:10.1080/08958370802526881
PMID:19225963
Abstract

The protective effect of diphenyl diselenide, (PhSe)(2), on oxidative stress induced by cigarette smoke exposure in brains of rat pups was evaluated. Animals were exposed to passive cigarette smoke (15 min/day) in two different experimental protocols: P1 (1, 2, and 3 cigarettes) and P2 (4, 5, and 6 cigarettes) for 3 weeks. Before each period of smoke exposure, animals received an oral administration of (PhSe)(2) (0.5 mg/kg). A number of toxicological parameters in the brain were examined, such as lipid peroxidation, delta-aminolevulinate dehydratase (delta-ALA-D) activity, and components of enzymatic (superoxide dismutase and catalase activities) and non-enzymatic antioxidant defenses (ascorbic acid and non-protein thiol levels). In P1, smoke exposure induced an inhibition of catalase activity and an increase of ascorbic acid levels. (PhSe)(2) treatment was able to protect catalase activity but not ascorbic acid levels. In P2, an augmentation of lipid peroxidation, a reduction of enzymatic and non-enzymatic antioxidant status, and an inhibition of delta-ALA-D activity caused by smoke exposure were found. (PhSe)(2) protected the brains of rat pups against oxidative damage induced by smoke exposure. The results are consistent with the antioxidant effect of (PhSe)(2) demonstrated by the reduction of oxidative changes caused by smoke exposure in the brains of pups.

摘要

评估了二苯基二硒醚((PhSe)(2))对暴露于香烟烟雾的幼鼠大脑中氧化应激的保护作用。动物在两种不同的实验方案中被动暴露于香烟烟雾(每天15分钟):方案P1(1、2和3支香烟)和方案P2(4、5和6支香烟),持续3周。在每次烟雾暴露前,动物口服(PhSe)(2)(0.5毫克/千克)。检测了大脑中的一些毒理学参数,如脂质过氧化、δ-氨基乙酰丙酸脱水酶(δ-ALA-D)活性以及酶促(超氧化物歧化酶和过氧化氢酶活性)和非酶促抗氧化防御(抗坏血酸和非蛋白硫醇水平)的成分。在方案P1中,烟雾暴露导致过氧化氢酶活性受到抑制,抗坏血酸水平升高。(PhSe)(2)处理能够保护过氧化氢酶活性,但不能保护抗坏血酸水平。在方案P2中,发现烟雾暴露导致脂质过氧化增加、酶促和非酶促抗氧化状态降低以及δ-ALA-D活性受到抑制。(PhSe)(2)保护幼鼠大脑免受烟雾暴露诱导的氧化损伤。这些结果与(PhSe)(2)的抗氧化作用一致,该作用通过减少幼鼠大脑中烟雾暴露引起的氧化变化得以证明。

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