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甲基苯丙胺与大鼠视网膜中的脂质过氧化作用

Methamphetamine and lipid peroxidation in the rat retina.

作者信息

Melo Pedro, Rodrigues Lorena G, Pinazo-Durán Maria Dolores, Tavares Maria Amélia

机构信息

Institute of Anatomy, Faculty of Medicine, University of Porto, Alameda Hernâni Monteiro, 4200-319 Porto, Portugal.

出版信息

Birth Defects Res A Clin Mol Teratol. 2005 Jun;73(6):455-60. doi: 10.1002/bdra.20138.

DOI:10.1002/bdra.20138
PMID:15880787
Abstract

BACKGROUND

The use of psychoactive drugs during adolescence and early adult life has increased in the last few decades. It is known that developmental exposure to psychostimulants affects the sensory systems, and the retina has been shown to be a target tissue. This work was conducted to evaluate the pattern of lipid peroxidation in the rat retina following prenatal exposure to methamphetamine (MA).

METHODS

Pregnant female Wistar rats were given MA (5 mg/kg of body weight/day; SC, in 0.9% saline) from GD 8 to 22. Offspring were sacrificed at postnatal days (PNDs) 7, 14, and 21. The retinas were homogenized, and both the total antioxidant and superoxide dismutase (SOD) activities were measured by enzymatic-colorimetric methods. The lipid peroxidation byproducts (malondialdehyde [MDA] and MDA-like metabolites) were measured by the thiobarbituric acid test.

RESULTS

Total antioxidant levels were lower in the MA group at PND 21 in both males and females. The activity of SOD was higher in PND 7 females from the MA group. MDA levels were higher in the MA group at PND 21 in both genders.

CONCLUSIONS

These findings suggest that prenatal-induced MA toxicity in the retina may be related to lipid peroxidation processes and oxidative stress.

摘要

背景

在过去几十年中,青少年和成年早期使用精神活性药物的情况有所增加。已知发育过程中接触精神兴奋剂会影响感觉系统,视网膜已被证明是一个靶组织。本研究旨在评估产前接触甲基苯丙胺(MA)后大鼠视网膜脂质过氧化的模式。

方法

妊娠雌性Wistar大鼠从妊娠第8天至第22天给予MA(5mg/kg体重/天;皮下注射,溶于0.9%生理盐水中)。在出生后第7天、第14天和第21天处死后代。将视网膜匀浆,采用酶比色法测定总抗氧化剂和超氧化物歧化酶(SOD)活性。通过硫代巴比妥酸试验测定脂质过氧化副产物(丙二醛[MDA]和MDA样代谢物)。

结果

在出生后第21天,MA组雄性和雌性大鼠的总抗氧化剂水平均较低。MA组出生后第7天雌性大鼠的SOD活性较高。在出生后第21天,MA组两性的MDA水平均较高。

结论

这些发现表明,产前MA诱导的视网膜毒性可能与脂质过氧化过程和氧化应激有关。

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