Warshawsky D, Cody T, Radike M, Reilman R, Schumann B, LaDow K, Schneider J
University of Cincinnati, Department of Environmental Health, OH 45267-0056, USA.
Chem Biol Interact. 1995 Jul 14;97(2):131-48. doi: 10.1016/0009-2797(95)03610-x.
This laboratory has shown that the metabolism of benzo[a]pyrene (BaP), a carcinogenic polycyclic aromatic hydrocarbon (PAH), by a freshwater green alga, Selenastrum capricornutum, under gold light proceeds through a dioxygenase pathway with subsequent conjugation and excretion. This study was undertaken to determine: (1) the effects of different light sources on the enzymatic or photochemical processes involved in the biotransformation of BaP over a dose range of 5-1200 mg/l; (2) the phototoxicity of carcinogenic PAHs and mutagenic quinones to a green alga; (3) the ability of other algal systems to metabolize BaP. Cultures were exposed to different doses of BaP for 2 days at 23 degrees C under gold, white or UV-A fluorescent light on a diurnal cycle of 16 h light, 8 h dark. Under gold light, metabolites of BaP produced by Selenastrum capricornutum were the dihydrodiols of which the 11,12-dihydrodiol was the major metabolite. Under white light, at low doses, the major metabolite was the 9,10-dihydrodiol. With increasing dose, the ratio of dihydrodiols to quinones decreased to less than two. With increasing light energy output, from gold to white to UV-A in the PAH absorbing region, BaP quinone production increased. Of other carcinogenic PAHs studied, only 7H-dibenz[c,g]carbazole was as phototoxic as BaP while 7,12-dimethylbenz[a]anthracene, dibenz[a,j]acridine and non-carcinogenic PAHs, anthracene and pyrene, were not phototoxic. The 3,6-quinone of BaP was found to be highly phototoxic while quinones that included menadione, danthron, phenanthrene-quinone and hydroquinone were not. The data suggest that the phototoxicity of BaP is due to photochemical production of quinones; the 3,6-quinone of BaP is phototoxic and is probably the result of the production of short lived cyclic reactive intermediates by the interaction of light with the quinone. Lastly, only the green algae, Selenastrum capricornutum, Scenedesmus acutus and Ankistrodesmus braunii almost completely metabolized BaP to dihydrodiols. The green alga Chlamydomonas reinhardtii, the yellow alga Ochromonas malhamensis, the blue green algae Anabaena flosaquae and euglenoid Euglena gracilis did not metabolize BaP to any extent. The data indicate that algae are important in their ability to degrade PAHs but the degradation is dependent on the dose of light energy emitted and absorbed, the dose of PAHs to which the algae are exposed, the phototoxicity of PAHs and their metabolite(s) and the species and strain of algae involved. All of these factors will be important in assessing the degradation and detoxification pathways of recalcitrant PAHs by algae.
本实验室已表明，淡水绿藻羊角月牙藻在金色光下对致癌多环芳烃苯并[a]芘（BaP）的代谢是通过双加氧酶途径进行的，随后进行结合和排泄。本研究旨在确定：（1）在5 - 1200 mg/l的剂量范围内，不同光源对BaP生物转化过程中所涉及的酶促或光化学过程的影响；（2）致癌多环芳烃和致突变醌类对绿藻的光毒性；（3）其他藻类系统代谢BaP的能力。培养物在23摄氏度下，于金色、白色或UV - A荧光灯下，以16小时光照、8小时黑暗的昼夜循环暴露于不同剂量的BaP中2天。在金色光下，羊角月牙藻产生的BaP代谢产物是二氢二醇，其中11,12 - 二氢二醇是主要代谢产物。在白色光下，低剂量时主要代谢产物是9,10 - 二氢二醇。随着剂量增加，二氢二醇与醌类的比例降至小于2。在多环芳烃吸收区域，随着光能输出从金色光增加到白色光再到UV - A光，BaP醌类的产量增加。在所研究的其他致癌多环芳烃中，只有7H - 二苯并[c,g]咔唑与BaP一样具有光毒性，而7,12 - 二甲基苯并[a]蒽、二苯并[a,j]吖啶以及非致癌多环芳烃蒽和芘则没有光毒性。发现BaP的3,6 - 醌具有高度光毒性，而包括甲萘醌、丹蒽醌、菲醌和对苯二酚在内的醌类则没有。数据表明，BaP的光毒性是由于醌类的光化学产生；BaP的3,6 - 醌具有光毒性，可能是光与醌相互作用产生短寿命环状反应中间体的结果。最后，只有绿藻羊角月牙藻、尖锐栅藻和布朗角星鼓藻几乎将BaP完全代谢为二氢二醇。莱茵衣藻、玛氏赭球藻、水华鱼腥藻和纤细裸藻没有在任何程度上代谢BaP。数据表明，藻类在降解多环芳烃的能力方面很重要，但降解取决于发射和吸收的光能剂量、藻类暴露于其中的多环芳烃剂量、多环芳烃及其代谢产物的光毒性以及所涉及的藻类物种和菌株。所有这些因素在评估藻类对难降解多环芳烃的降解和解毒途径时都将很重要。
