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二苯基二硒醚可预防香烟烟雾暴露诱导的新生大鼠肺氧化损伤。

Diphenyl diselenide prevents oxidative damage induced by cigarette smoke exposure in lung of rat pups.

作者信息

Luchese Cristiane, Stangherlin Eluza C, Ardais Ana P, Nogueira Cristina W, Santos Francielli W

机构信息

Departamento de Química, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, Santa Maria, CEP 97105-900, RS, Brazil.

出版信息

Toxicology. 2007 Feb 12;230(2-3):189-96. doi: 10.1016/j.tox.2006.11.051. Epub 2006 Nov 19.

DOI:10.1016/j.tox.2006.11.051
PMID:17178183
Abstract

The effect of cigarette smoke exposure on lungs of rat pups was evaluated. Animals were exposed to passive cigarette smoke during 3 weeks and a number of toxicological parameters in lung of pups were examined, such as lipid peroxidation, delta-aminolevulic acid dehydratase (delta-ALA-D) activity, components of the enzymatic antioxidant defenses (superoxide dismutase (SOD) and catalase activities) and non-enzymatic antioxidant defenses (Vitamin C and non-protein thiol (NPSH) levels). Furthermore, a possible protective effect of diphenyl diselenide, (PhSe)(2), was studied. The results demonstrated an increase in lipid peroxidation, an inhibition of delta-ALA-D activity, a reduction of Vitamin C and NPSH levels induced by cigarette smoke exposure, indicating damage in lungs of rat pups. Oral administration of (PhSe)(2) (0.5mg/kg) restored TBARS levels, non-enzymatic antioxidant defenses and activity of delta-ALA-D. These results indicated that exposure to cigarette smoke enhanced oxidative stress, thereby disturbing the tissue defense system. (PhSe)(2) protected against oxidative damage induced by cigarette smoke exposure in lung of rat pups.

摘要

评估了香烟烟雾暴露对幼鼠肺部的影响。动物在3周内暴露于被动香烟烟雾中,并检测了幼鼠肺部的一些毒理学参数,如脂质过氧化、δ-氨基乙酰丙酸脱水酶(δ-ALA-D)活性、酶促抗氧化防御成分(超氧化物歧化酶(SOD)和过氧化氢酶活性)以及非酶促抗氧化防御(维生素C和非蛋白硫醇(NPSH)水平)。此外,还研究了二苯基二硒化物(PhSe)₂的可能保护作用。结果表明,香烟烟雾暴露导致脂质过氧化增加、δ-ALA-D活性受到抑制、维生素C和NPSH水平降低,表明幼鼠肺部受到损伤。口服(PhSe)₂(0.5mg/kg)可恢复硫代巴比妥酸反应物(TBARS)水平、非酶促抗氧化防御以及δ-ALA-D的活性。这些结果表明,暴露于香烟烟雾会增强氧化应激,从而扰乱组织防御系统。(PhSe)₂可保护幼鼠肺部免受香烟烟雾暴露诱导的氧化损伤。

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