Programa de Pós Graduação em Farmacologia - UFSM, Brazil.
Departamento de Fisiologia e Farmacologia - UFSM, Brazil.
Aquat Toxicol. 2014 Dec;157:175-85. doi: 10.1016/j.aquatox.2014.10.015. Epub 2014 Oct 27.
The aim of this study was to assess the Mn toxicity to silver catfish considering Mn accumulation and oxidative status in different tissues, as well as pituitary hormone expression after acclimation to hypoxia. Silver catfish acclimated to hypoxia for 10 days and successively exposed to Mn (9.8 mg L(-1)) for an additional 10 days exhibited lower Mn accumulation in plasma, liver, kidneys and brain and prevented the hematocrit decrease observed in the normoxia group. Hypoxia acclimation also modified Mn-induced oxidative damage, which was observed by lower reactive species (RS) generation in gills and kidneys, decreased lipid peroxidation (LP) levels in gills, liver and kidneys and decreased protein carbonyl (PC) levels in liver, kidneys and brain. Manganese accumulation showed positive correlations with LP levels in gills and kidneys, as well as with PC levels in gills, liver and brain. In addition, hypoxia acclimation and Mn exposure increased catalase (CAT) activity in gills and kidneys and Na(+)/K(+)-ATPase activity in gills, liver and brain. Silver catfish that were acclimated under normoxia and exposed to Mn displayed increased pituitary prolactin (PRL) and decreased somatolactin (SL) expression. Interestingly, hypoxia acclimation prevented hormonal fluctuation of PRL and SL in fish exposed to Mn. These findings indicate that while the exposure of silver catfish to Mn under normoxia was related to metal accumulation and oxidative damage in tissues together with endocrine axis disruption, as represented by PRL and SL, hypoxia acclimation reduced waterborne Mn uptake, thereby minimizing oxidative damage and changes in hormonal profile. We hypothesized that moderate hypoxia is able to generate adaptive responses, which may be related to hormesis, thereby ameliorating Mn toxicity to silver catfish.
本研究旨在评估锰对银鲶的毒性，考虑到在适应低氧后不同组织中的锰积累和氧化状态，以及垂体激素表达。银鲶适应低氧 10 天后，连续暴露于锰（9.8mg/L）10 天，血浆、肝脏、肾脏和大脑中的锰积累较低，并防止了在常氧组中观察到的血细胞比容下降。低氧适应还改变了锰诱导的氧化损伤，这表现在鳃和肾脏中活性物质（RS）生成减少，鳃、肝脏和肾脏中脂质过氧化（LP）水平降低，以及肝脏、肾脏和大脑中蛋白质羰基（PC）水平降低。锰积累与鳃和肾脏中的 LP 水平以及鳃、肝脏和大脑中的 PC 水平呈正相关。此外，低氧适应和锰暴露增加了鳃和肾脏中的过氧化氢酶（CAT）活性以及鳃、肝脏和大脑中的 Na(+)/K(+)-ATP 酶活性。在常氧下适应并暴露于锰的银鲶显示催乳素（PRL）增加和生长激素（SL）减少。有趣的是，低氧适应防止了暴露于锰的鱼类中 PRL 和 SL 的激素波动。这些发现表明，当银鲶在常氧下暴露于锰时，与组织中的金属积累和氧化损伤以及内分泌轴的破坏有关，如 PRL 和 SL 所示，低氧适应减少了水锰的摄取，从而最小化氧化损伤和激素谱的变化。我们假设适度的低氧能够产生适应反应，这可能与毒物兴奋效应有关，从而改善银鲶的锰毒性。
