Large amounts of aluminum (Al) are found in wastewater from industrial bauxite mining, which is often responsible for the contamination of drinking water sources in urban and rural communities. Although this metal exhibits broad environmental distribution, its cardiac repercussions are poorly understood, making it difficult to establish diagnostic criteria in cases of Al intoxication. In the absence of clinical data, we used a preclinical model to investigate the impact of Al exposure on heart bioaccumulation, molecular oxidation, micromineral distribution, structural and ultrastructural remodeling of the cardiac tissue. Male Wistar rats were equally randomized into five groups: G1 = distilled water; and G2 to G5 = 0.02, 0.1, 50, and 200 mg/kg aluminum solution, respectively. After 120 days, the hearts were collected and subjected to mineral microanalysis, immunoenzymatic detection of 8-OHdG, as well as bright field, polarizing, scanning and transmission electron microscopy to estimate the extent of the cardiac remodeling and cardiomyocytes ultrastructure. Long-term Al exposure induced dose-dependent bioaccumulation, micromineral imbalance, genomic DNA oxidation, structural and ultrastructural abnormalities of the cardiac tissue, resulting in extensive parenchymal loss, stromal expansion, diffuse inflammatory infiltrate, increased glycoconjugate and collagen deposition, subversion and collapse of the collagen network, reduced myocardial vascularization index, mitochondrial swelling, sarcomere disorganization, myofilament dissociation, and fragmentation in cardiomyocytes. Our findings indicated that the heart was sensitive to Al-mediated toxicity, especially in animals treated with the three highest doses of Al. In response to Al-induced loss of the parenchyma, heart stroma exhibited a reactive and compensatory expansion, which, in combination with the increased distribution of thick myofibrils and degenerated mitochondria in cardiomyocytes, provides morphological evidence that cardiac tissue adaptations are not enough to adjust the relationships between the parenchyma and stroma until a steady state is reached, resulting in continuous pathological remodeling potentially associated with Al-induced proinflammatory and pro-oxidant events.

在工业铝土矿开采的废水中发现大量的铝（Al），通常是造成城市和农村社区饮用水源污染的原因。尽管这种金属表现出广泛的环境分布，但是人们对其心脏的反应知之甚少，因此难以确定铝中毒的诊断标准。在缺乏临床数据的情况下，我们使用临床前模型来研究铝暴露对心脏生物蓄积，分子氧化，微量矿物质分布，心脏组织的结构和超微结构重塑的影响。将雄性Wistar大鼠平均分为5组：G1 =蒸馏水； G1 =蒸馏水。和G2至G5分别为0.02、0.1、50和200 mg / kg铝溶液。120天后，收集心脏并进行矿物质微分析，8-OHdG的免疫酶检测以及明场，极化，扫描和透射电镜，以评估心脏重塑和心肌细胞超微结构的程度。长期暴露于铝导致剂量依赖性生物蓄积，微量矿物质失衡，基因组DNA氧化，心脏组织的结构和超微结构异常，导致大量实质损失，间质扩张，弥漫性炎症浸润，糖结合物和胶原蛋白沉积增加，破坏和塌陷胶原网络，减少的心肌血管化指数，线粒体肿胀，肌节紊乱，肌丝解离和心肌细胞破碎。我们的发现表明，心脏对铝介导的毒性敏感，尤其是在接受三种最高剂量的铝治疗的动物中。响应于Al引起的实质损失，心脏基质表现出反应性和代偿性扩张，再加上心肌细胞中浓厚的肌原纤维和线粒体变性的分布增加，提供了形态学证据，表明心脏组织适应性不足以调节心肌组织薄壁组织与间质之间的关系直到达到稳定状态，导致持续的病理重塑可能与铝诱导的促炎和促氧化事件有关。