Laboratório de Metabolismo e Reprodução de Organismos Aquáticos, Departamento de Fisiologia, Instituto de Biociências, Universidade de São Paulo, Rua do Matão, travessa 14, n.321, São Paulo, SP, Brazil.
Laboratório de Ecofisiologia Animal, Departamento de Ciências Fisiológicas, Universidade Estadual de Londrina, Londrina, Paraná, Brazil.
Comp Biochem Physiol C Toxicol Pharmacol. 2019 Jan;215:33-40. doi: 10.1016/j.cbpc.2018.09.004. Epub 2018 Oct 11.
Exposure to aluminum (Al) and aluminum + manganese (Mn) can trigger an increase in reactive oxygen species (ROS) and modify the activity of oxidative defense enzymes. This study investigated whether exposure to Al and Al + Mn at acid pH for 24 and 96 h causes oxidative stress evidenced by antioxidants and oxidative damage in the gills and liver of sexually mature Astyanax altiparanae males. The fish were subsequently immersed in metal-free water for 24 and 96 h to see whether they recovered from the effects of these metals. Exposure to an acid pH boosted the activity of gill superoxide dismutase (SOD) at 96 h and the fish did not recover when immersed for the same period in water at neutral pH. Exposure to Al increased glutathione (GSH) levels (24 h) in the gills, returning to control levels during the recovery period, showing the efficiency of the antioxidant system in preventing lipid peroxidation of the gills and liver. Mn did not modify the activity of the enzymes studied, but did trigger late hepatic lipid peroxidation during the recovery period. The group exposed to Al + Mn exhibited several alterations, including increased concentration of GSH, as well as higher GPx and GR activity in the gills. Despite the defensive responses triggered by acute exposure, during the recovery period there were alterations in catalase (96 h) and an increase in hepatic metallothionein (24 h), but this did not prevent hepatic lipid peroxidation. Al and Al + Mn produced different effects, and the timing of enzymatic and non-enzymatic antioxidant defenses also differed.
暴露于铝(Al)和铝+锰(Mn)会引发活性氧(ROS)的增加,并改变氧化防御酶的活性。本研究调查了在酸性 pH 值下暴露于 Al 和 Al+Mn 24 和 96 小时是否会导致性成熟 Astyanax altiparanae 雄性鱼鳃和肝脏中的抗氧化剂和氧化损伤引起的氧化应激。随后,将鱼浸入无金属水中 24 和 96 小时,以观察它们是否从这些金属的影响中恢复过来。暴露于酸性 pH 值会在 96 小时时增加鳃中超氧化物歧化酶(SOD)的活性,而当鱼在中性 pH 值的水中浸泡相同时间时,它们不会恢复。暴露于 Al 会在 24 小时时增加鳃中谷胱甘肽(GSH)的水平,在恢复期间恢复到对照水平,表明抗氧化系统在防止鳃和肝脏脂质过氧化方面的效率。Mn 没有改变研究中酶的活性,但在恢复期间会引发迟发性肝脂质过氧化。暴露于 Al+Mn 的组表现出多种改变,包括 GSH 浓度增加,以及鳃中的 GPx 和 GR 活性升高。尽管急性暴露引发了防御反应,但在恢复期间,过氧化氢酶(96 小时)发生改变,并且肝金属硫蛋白(24 小时)增加,但这并不能防止肝脂质过氧化。Al 和 Al+Mn 产生了不同的影响,并且酶和非酶抗氧化防御的时间也不同。