氯霉素对费氏弧菌0~24 h的Hormesis 效应及其机制初探

为了探究抗生素对发光菌的Hormesis效应，选择费氏弧菌（Vibrio fischeri, V.fischeri）为受试生物，氯霉素为研究对象，测定了0~24 h下氯霉素对V.fischeri的发光强度（Hv）及生长量（OD600）的作用，探讨氯霉素对V.fischeri的低浓度促进效应及其可能机制.结果表明，氯霉素对V.fischeri的发光强度具有明显的促进作用，且仅出现在细菌生长的延滞期.根据V.fischeri的发光机制，结合Gaussian量子化学计算结果，即氯霉素的最正氢电荷为0.244，远大于烟酰胺腺嘌呤二核苷酸（NADH）的最正氢电荷0.135，提出氯霉素通过提供质子促进荧光反应，进而产生Hormesis效应的可能机制.
In order to reveal the Hormesis effect of antibiotics on bacterial, the adverse effects of chloramphenicol on the luminescence and cell proliferation (0 to 24 h) of Vibrio fischeri (V.fischeri) were investigated. It was found that an obvious stimulation effect at the low concentration would occur on the luminescence intensity at the lag phase of V.fischeri under the action of chloramphenicol. A possible mechanism hypothesis of the stimulation effect was then proposed, based on the light emitting mechanisms and the quantum chemical parameters calculated by Gaussian 09. It was supposed that because of a higher value of the most positive charge of the H atoms of chloramphenicol than NADH, chloramphenicol could act as proton donors to provide protons which were essential for the light emitting process, instead of NADH, and stimulated the light emitting of the bacteria