Gagné F, André C, Cejka P, Gagnon C, Blaise C
St. Lawrence Centre, Environment Canada, 105 Mc Gill, Montréal, Quebec, Canada.
Comp Biochem Physiol C Toxicol Pharmacol. 2007 May;145(4):542-52. doi: 10.1016/j.cbpc.2007.01.019. Epub 2007 Feb 22.
This study examined the toxic potential of a primary-treated municipal effluent, before and after ozonation, in freshwater mussels. Animals were exposed to various concentrations (0, 1, 3, 10 and 20% v/v) of a primary-treated effluent and also after a treatment with ozone at 10 mg/L in continuous flow-through mode for seven weeks. A suite of biomarkers was used to assess the potential toxic effects of various contaminants typically present in municipal wastewaters: heavy metal metabolism (metallothioneins and labile zinc), cytochrome P4501A1 and 3A4, glutathione S-transferase activities (biotransformation of organic compounds), lipid peroxidation and xanthine oxidoreductase (oxygen radical scavenging), DNA damage, mitochondrial electron transport activity at various temperatures and gonad lipid levels (cellular energy allocation) and aspartate transcarbamoylase and dihydrofolate reductase (gonad activity). On the one hand, some biomarkers, including metallothioneins, labile zinc, glutathione S-transferase, cytochrome P4503A4 activity, dehydrofolate reductase and aspartate transcarbamoylase, were readily decreased. In contrast, these biomarkers, cytochrome P4501A1, gill lipid peroxidation, DNA strand breaks in gills and digestive gland, mitochondrial electron transport at high and low temperatures (temperature-dependent activity) and total gonad lipids, were readily increased. In general, ozone treatment reduced adverse effects by either decreasing the intensity of the toxic responses or increasing the threshold concentration. For gill lipid peroxidation, however, intensity was greater at a higher threshold concentration. Ozone treatment eliminated the temperature sensitivity of the mitochondrial electron transport system, indicating a loss of interaction between temperature and urban pollution in terms of energy expenditure in mussels. Ozone treatment could significantly decrease either the toxic potency or intensity of urban pollutants at the expense of increased oxidative stress in gills of freshwater mussels.
本研究检测了初级处理后的城市污水在臭氧化前后对淡水贻贝的潜在毒性。将动物暴露于不同浓度(0、1、3、10和20% v/v)的初级处理污水中,以及在连续流通模式下用10 mg/L臭氧处理后的污水中,持续7周。使用一系列生物标志物来评估城市污水中通常存在的各种污染物的潜在毒性作用:重金属代谢(金属硫蛋白和不稳定锌)、细胞色素P4501A1和3A4、谷胱甘肽S-转移酶活性(有机化合物的生物转化)、脂质过氧化和黄嘌呤氧化还原酶(氧自由基清除)、DNA损伤、不同温度下的线粒体电子传递活性和性腺脂质水平(细胞能量分配)以及天冬氨酸转氨甲酰酶和二氢叶酸还原酶(性腺活性)。一方面,一些生物标志物,包括金属硫蛋白、不稳定锌、谷胱甘肽S-转移酶、细胞色素P4503A4活性、二氢叶酸还原酶和天冬氨酸转氨甲酰酶,很容易降低。相比之下,这些生物标志物,细胞色素P4501A1、鳃脂质过氧化、鳃和消化腺中的DNA链断裂、高温和低温下的线粒体电子传递(温度依赖性活性)以及总性腺脂质,很容易增加。一般来说,臭氧处理通过降低毒性反应强度或提高阈值浓度来减少不利影响。然而,对于鳃脂质过氧化,在较高阈值浓度下强度更大。臭氧处理消除了线粒体电子传递系统的温度敏感性,表明在贻贝能量消耗方面温度与城市污染之间的相互作用丧失。臭氧处理可以显著降低城市污染物的毒性效力或强度,但代价是淡水贻贝鳃中氧化应激增加。