抗生素引起的线粒体变化可能导致致癌。

Jorma Jyrkkanen
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摘要

真核生物中的线粒体是一种原始的内共生细菌,与现存的SARII海洋细菌和立克次体有关,负责氧化磷酸化(OP)、ATP和NAD的产生。当暴露于临床等量的靶向细菌抗生素(环丙霉素、氨苄西林、卡那霉素)时,会表现出谷胱甘肽滴度下降、活性氧(ROS)增加和过氧化脂质增加[1,2]。抗生素对线粒体和微生物组的作用方式喹诺酮类:常用的抗菌有机氟化合物,通过抑制细菌DNA合成而导致细胞快速死亡。它们可能会对线粒体和人类微生物群造成附带损害。该组含有氧氟沙星、诺氟沙星(诺罗辛)、环丙沙星(环普罗)、莫西沙星(阿维洛)
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Antibiotic induced changes to mitochondria result in potential contributions to carcinogenesis.
Mitochondrial job and creation of toxic mix by antibiotic Mitochondria, a primitive endosymbiotic bacteria, related to extant SARII marine bacteria and Rickettsias, in eukaryotes is responsible for Oxidative Phosphorylation (OP) and ATP and NAD production, when exposed to clinically equivalent doses of antibiotics that target bacteria (cipromycin, ampicillin, kanamycin), exhibited a decline in glutathione titre, an increase in Reactive Oxygen (ROS) and an increase in lipid peroxide [1,2]. Modes of action of antibiotics on mitochondria and microbiome 1. Quinolones: Commonly prescribed antibacterial organofluorine compounds that act by inhibition of bacterial DNA synthesis and result in rapid cell death [3]. They could be expected to do collateral damage to mitochondria and the human microbiome. This group contains Ofloxacin, Norfloxacin (Noroxin), Ciprofloxacin (Cipro), Moxifloxacin (Avelox)
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