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褪黑素可降低快速老化小鼠红细胞和血浆中的氧化应激水平。

Melatonin reduces oxidative stress in erythrocytes and plasma of senescence-accelerated mice.

作者信息

Nogués M Rosa, Giralt Montserrat, Romeu Marta, Mulero Miquel, Sánchez-Martos Vanesa, Rodríguez Esperanza, Acuña-Castroviejo Darío, Mallol Jordi

机构信息

Unit of Pharmacology, School of Medicine and Health Sciences, Rovira i Virgili University, Reus, Spain.

出版信息

J Pineal Res. 2006 Sep;41(2):142-9. doi: 10.1111/j.1600-079X.2006.00344.x.

DOI:10.1111/j.1600-079X.2006.00344.x
PMID:16879320
Abstract

It has been suggested that oxidative stress is a feature of aging. The goal of the present study was to assess the oxidant effects related to aging and the protective role of exogenous melatonin in senescence-accelerated mice (SAMP8). Two groups of SAMP8 mice (males and females) were compared with their respective control groups of SAMR1 mice (senescence-resistant inbred strain) to determine their oxidative status without melatonin treatment. Four other groups of the same characteristics were treated with melatonin (10 mg/kg/day) in their drinking water. The melatonin concentration in the feeding bottles was titrated according to water consumption and body weight (i.e. 0.06 mg/mL for 30 g of body weight and 5 mL/day of water consumption). The treatment began when animals were 1-month old and continued for 9 months. When mice were 10-month old, they were anesthetized and blood was obtained. Plasma and erythrocytes were processed to examine oxidative stress markers: reduced glutathione (GSH), oxidized glutathione (GSSG), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione reductase (GR), glutathione S-transferase (GST), thiobarbituric acid reactive substances (TBARS), and hemolysis. The results showed greater oxidative stress in SAMP8 than in SAMR1, largely because of a decrease in GSH levels and to an increase in GSSG and TBARS with the subsequent induction of the antioxidant enzymes GPX and GR. Melatonin, as an antioxidant molecule, improved the glutathione-related parameters, prevented the induction of GPX in senescent groups, and promoted a decrease in SOD and TBARS in almost all the groups.

摘要

有人提出氧化应激是衰老的一个特征。本研究的目的是评估与衰老相关的氧化作用以及外源性褪黑素在衰老加速小鼠(SAMP8)中的保护作用。将两组SAMP8小鼠(雄性和雌性)与其各自的SAMR1小鼠对照组(抗衰老近交系)进行比较,以确定在不进行褪黑素处理的情况下它们的氧化状态。另外四组具有相同特征的小鼠在饮用水中添加褪黑素(10毫克/千克/天)进行处理。根据饮水量和体重调整喂水瓶中褪黑素的浓度(即体重30克且每日饮水量5毫升时为0.06毫克/毫升)。处理从动物1月龄开始,持续9个月。当小鼠10月龄时,将其麻醉并采集血液。对血浆和红细胞进行处理以检测氧化应激标志物:还原型谷胱甘肽(GSH)、氧化型谷胱甘肽(GSSG)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPX)、谷胱甘肽还原酶(GR)、谷胱甘肽S-转移酶(GST)、硫代巴比妥酸反应性物质(TBARS)以及溶血情况。结果显示,SAMP8小鼠的氧化应激比SAMR1小鼠更严重,这主要是由于GSH水平降低以及GSSG和TBARS增加,随后诱导了抗氧化酶GPX和GR。褪黑素作为一种抗氧化分子,改善了与谷胱甘肽相关的参数,防止了衰老组中GPX的诱导,并使几乎所有组中的SOD和TBARS都有所降低。

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