受重金属污染的新热带河流中鲈鱼的组织病理学以及金属硫蛋白、热休克蛋白和诱导型一氧化氮合酶的表达变化。

Alessandro Loureiro Paschoalini, Yves Moreira Ribeiro, Breno Thuller, Camila Leandro Gomes Soares, Elizete Rizzo, Nilo Bazzoli
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引用次数: 0

摘要

巴西最近发生的大坝溃坝事故向帕拉奥佩巴河上游排放了数吨采矿尾矿,对这条河流造成了前所未有的影响。本研究旨在评估大坝溃坝四年后重金属对巴西重要商业鱼种 Prochilodus costatus 的影响。为此,研究人员分析了重金属、氧化应激和环境压力的生物标志物,并对目标器官进行了组织学分析。结果表明,帕拉奥佩巴河的鱼类受到严重污染。据观察,成本鲈的金属硫蛋白(MTs)、热休克蛋白(HSP70)和诱导型一氧化氮合酶(iNOS)的表达量增加,肝脏、脾脏和性腺的组织学变化率也更高。这些发现表明,尽管过去曾受到污染,但采矿尾矿中的金属已大大加剧了帕拉奥佩巴河流域的污染。
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Histopathology and changes in the expression of metallothioneins, heat shock proteins and inducible nitric oxide synthase in Prochilodus costatus from a neotropical river contaminated by heavy metals.

The most recent dam rupture in Brazil released tons of mining tailings into the upper course of the Paraopeba River, affecting this river in an unprecedented way. The present study aimed to evaluate the influence of heavy metals on Prochilodus costatus, an important commercial species in Brazil, four years after the dam colapse. To this end, biomarkers of heavy metals, oxidative stress, and environmental stress were analyzed, and histological analyses of target organs were performed. The results demonstrated critical contamination of fish from the Paraopeba River. Increased expression of Metallothioneins - MTs, Heat Shock Protein - HSP70, and inducible nitric oxide synthase - iNOS, as well as greater rates of histological changes in the liver, spleen, and gonads, were observed in P. costatus. These findings demonstrate that, despite past contamination, the metals present in mining tailings have significantly increased the contamination of the Paraopeba River basin.

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Histopathology and changes in the expression of metallothioneins, heat shock proteins and inducible nitric oxide synthase in Prochilodus costatus from a neotropical river contaminated by heavy metals. Chlorpyrifos-induced suppression of the antioxidative defense system leads to cytotoxicity and genotoxicity in macrophages. Gene expression profiles and protein-protein interaction networks in THP-1 cells exposed to metal-based nanomaterials. N-Acetyl-L-Cysteine Attenuates Titanium Dioxide Nanoparticle (TiO2 NP)-Induced Autophagy in Male Germ Cells. PM2.5 induces cardiac defects via AHR-SIRT1-PGC-1α mediated mitochondrial damage
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