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抗坏血酸对抗癌药物诱导的氧化应激和基因毒性损伤的保护作用 。 你提供的原文似乎不完整,“in”后面缺少具体内容。

Protective effects of ascorbic acid against anticancer drug-induced oxidative stress and genotoxic damage in .

作者信息

da Mata Ana Maria Oliveira Ferreira, Silva Reyca Rodrigues E, Braga Antônio Lima, de Carvalho Ricardo Melo, de Oliveira Santos José Victor, de Alencar Marcus Vinícius Oliveira Barros, Paz Márcia Correia Fernanda Jardim, Ansari Siddique Akber, Ansari Irfan Aamer, Islam Muhammad Torequl, de Castro E Sousa João Marcelo, da Silva Felipe Cavalcanti Carneiro, de Carvalho Melo Cavalcante Ana Amélia, da Silva Benedito Borges

机构信息

Northeast Biotechnology Network (RENORBIO), Postgraduate Program in Biotechnology, Federal University of Piauí-UFPI, Teresina, Piauí 64049-550 Brazil.

Laboratory of Genetics and Toxicology-LAPGENIC, Post-Graduate Program in Pharmaceutical Science, Federal University of Piauí, Teresina, Piauí 64049-550 Brazil.

出版信息

3 Biotech. 2025 May;15(5):118. doi: 10.1007/s13205-025-04280-y. Epub 2025 Apr 7.

Abstract

The widely used dietary antioxidant ascorbic acid (AA) is evident to possess protective effects against many chronic diseases. This study aimed to evaluate the effects of AA on oxidative stress and genotoxic damage caused by 5-fluorouracil (5-FU), docetaxel (DOCE), and tamoxifen (TAMOX) in two proficient and four isogenic strains. For this, we performed disc diffusion and comet alkaline assay using suitable standard drugs. The results suggest that 5-FU, DOCE, TAMOX, and their combinations induced significant oxidative damage (p < 0.001) in all strains. These anticancer drugs and their combinations also induced genotoxicity (p < 0.05) in the SODWT strain when compared to the negative control group. These drugs and their combinations augmented damage index (ID) and damage frequency (FD) in the comet assay. However, AA alone, as well as when co-treated with these anticancer drugs, significantly (p < 0.05) reduced the damaging effects (oxidative stress and genotoxicity) on all test strains. AA showed the highest damage modulation with TAMOX (ID = 51.4% and FD = 50%), followed by 5-FU + DOCE (ID = 43.5% and FD = 42.9%), DOCE (ID = 42.5% and FD = 39.1%), and 5-FU + TAMOX (ID = 37% and FD = 33.6%), respectively. Taken together, AA reduced oxidative stress caused by the inducer hydrogen peroxide and showed anti-genotoxic activities against 5-FU, DOCE, and TAMOX, and their combinations mediated genotoxic effects on strains. Further studies are necessary to understand the molecular interference of AA in cancer therapies.

摘要

广泛使用的膳食抗氧化剂抗坏血酸(AA)显然对许多慢性疾病具有保护作用。本研究旨在评估AA对5-氟尿嘧啶(5-FU)、多西他赛(DOCE)和他莫昔芬(TAMOX)在两个近交系和四个同基因系中引起的氧化应激和遗传毒性损伤的影响。为此,我们使用合适的标准药物进行了纸片扩散法和彗星碱性试验。结果表明,5-FU、DOCE、TAMOX及其组合在所有品系中均诱导了显著的氧化损伤(p < 0.001)。与阴性对照组相比,这些抗癌药物及其组合在SODWT品系中也诱导了遗传毒性(p < 0.05)。这些药物及其组合在彗星试验中增加了损伤指数(ID)和损伤频率(FD)。然而,单独使用AA以及与这些抗癌药物联合处理时,均显著(p < 0.05)降低了对所有测试品系的损伤作用(氧化应激和遗传毒性)。AA对TAMOX的损伤调节作用最高(ID = 51.4%,FD = 50%),其次是5-FU + DOCE(ID = 43.5%,FD = 42.9%)、DOCE(ID = 42.5%,FD = 39.1%)和5-FU + TAMOX(ID = 37%,FD = 33.6%)。综上所述,AA降低了诱导剂过氧化氢引起的氧化应激,并对5-FU、DOCE和TAMOX及其组合介导的品系遗传毒性作用表现出抗遗传毒性活性。有必要进一步研究以了解AA在癌症治疗中的分子干扰作用。

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