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二苯甲基硒氰酸酯通过抗氧化和抑制 DNA 损伤减轻孔雀石绿诱导的氧化损伤在小鼠体内。

Diphenylmethyl selenocyanate attenuates malachite green induced oxidative injury through antioxidation & inhibition of DNA damage in mice.

机构信息

Department of Cancer Chemoprevention, Chittaranjan National Cancer Institute, Kolkata, India.

出版信息

Indian J Med Res. 2013 Jun;137(6):1163-73.

PMID:23852297
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3734721/
Abstract

BACKGROUND & OBJECTIVES: Malachite green (MG), an environmentally hazardous material, is used as a non permitted food colouring agent, especially in India. Selenium (Se) is an essential nutritional trace element required for animals and humans to guard against oxidative stress induced by xenobiotic compounds of diverse nature. In the present study, the role of the selenium compound diphenylmethyl selenocyanate (DMSE) was assessed on the oxidative stress (OS) induced by a food colouring agent, malachite green (MG) in vivo in mice.

METHODS

Swiss albino mice (Mus musculus) were intraperitoneally injected with MG at a standardized dose of 100 μg/ mouse for 30 days. DMSE was given orally at an optimum dose of 3 mg/kg b.w. in pre (15 days) and concomitant treatment schedule throughout the experimental period. The parameters viz. ALT, AST, LPO, GSH, GST, SOD, CAT, GPx, TrxR, CA, MN, MI and DNA damage have been evaluated.

RESULTS

The DMSE showed its potential to protect against MG induced hepatotoxicity by controlling the serum alanine aminotransferase and aspartate amino transferase (ALT and AST) levels and also ameliorated oxidative stress by modulating hepatic lipid peroxidation and different detoxifying and antioxidative enzymes such as glutathione-S-transferase (GST), superoxide dismutase (SOD), catalase (CAT), and also the selenoenzymes such as glutathione peroxidase (GPx) and thioredoxin reductase (TrxR) and reduced glutathione level which in turn reduced DNA damage.

INTERPRETATION & CONCLUSIONS: The organo-selenium compound DMSE showed significant protection against MG induced heptotoxicity and DNA damage in murine model. Better protection was observed in pretreatment group than in the concomitant group. Further studies need to be done to understand the mechanism of action.

摘要

背景与目的

孔雀石绿(MG)是一种对环境有害的物质,被用作非允许的食品着色剂,尤其是在印度。硒(Se)是动物和人类必需的营养微量元素,用于抵御各种性质的外源性化合物引起的氧化应激。在本研究中,评估了二苯甲基硒氰酸酯(DMSE)这种硒化合物对体内食物着色剂孔雀石绿(MG)诱导的氧化应激(OS)的作用。

方法

将瑞士白化小鼠(Mus musculus)用标准化剂量 100μg/只的 MG 腹膜内注射 30 天。DMSE 以最佳剂量 3mg/kg bw 在预(15 天)和整个实验期间同时进行治疗。评估了 ALT、AST、LPO、GSH、GST、SOD、CAT、GPx、TrxR、CA、MN、MI 和 DNA 损伤等参数。

结果

DMSE 通过控制血清丙氨酸氨基转移酶和天冬氨酸氨基转移酶(ALT 和 AST)水平,显示出其抵抗 MG 诱导的肝毒性的潜力,还通过调节肝脂质过氧化和不同的解毒和抗氧化酶,如谷胱甘肽-S-转移酶(GST)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、以及硒酶如谷胱甘肽过氧化物酶(GPx)和硫氧还蛋白还原酶(TrxR)和还原型谷胱甘肽水平,减轻了氧化应激,从而降低了 DNA 损伤。

解释与结论

有机硒化合物 DMSE 对 MG 诱导的小鼠模型肝毒性和 DNA 损伤表现出显著的保护作用。预处理组的保护效果优于同时处理组。需要进一步研究以了解其作用机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df92/3734721/da0fe3a6b140/IJMR-137-1163-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df92/3734721/1fe86480b4ff/IJMR-137-1163-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df92/3734721/91990fb0102b/IJMR-137-1163-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df92/3734721/0b977343b99c/IJMR-137-1163-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df92/3734721/da0fe3a6b140/IJMR-137-1163-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df92/3734721/1fe86480b4ff/IJMR-137-1163-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df92/3734721/91990fb0102b/IJMR-137-1163-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df92/3734721/0b977343b99c/IJMR-137-1163-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df92/3734721/da0fe3a6b140/IJMR-137-1163-g004.jpg

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