Griffin Gabrielle, Delnicki Morgan E, Lu Haiyan, Meaza Idoia, Williams Aggie, Vielee Samuel T, Bolatimi Oluwanifemi Esther, Wise Rachel M, Liu Rui, Kouokam J Calvin, Wise Sandra S, Wise John Pierce, Cave Matthew C, Wise John P, Wise Jamie Lynn
Department of Pharmacology and Toxicology, University of Louisville, Louisville, KY, United States.
Department of Pharmacology and Toxicology, University of Louisville, Louisville, KY, United States; Wise Laboratory of Environmental and Genetic Toxicology, Department of Pharmacology and Toxicology, University of Louisville, Louisville, KY, United States.
J Trace Elem Med Biol. 2025 Aug 23;91:127731. doi: 10.1016/j.jtemb.2025.127731.
Ranked as a "top 10 cause of death", chronic liver disease accounts for millions of deaths annually. The prevalence of the most prominent liver disease, metabolic dysfunction-associated steatotic liver disease (MASLD), has doubled over the past 20 years and continues to rise. Growing in parallel are environmental chemical exposures, emergingas key risk factors for liver disease. Hexavalent chromium [Cr(VI)] is the #1 chemical hazard in U.S. drinking water and is associated with increased liver disease incidence, including liver cancer. How Cr(VI) contributes to liver disease is poorly understood and no studies have considered whether Cr(VI) exposure together with high-fat diet, a well-established MASLD risk factor, drives liver disease. Thus, we developed an in vivo model to study the impact of Cr(VI) and high-fat diet on MASLD. Male Sprague Dawley rats were exposed to Cr(VI) in drinking water (0, 0.05, or 0.1 mg/L - levels that reflect the World Health Organization and U.S. Environmental Protection Agency maximum contaminant levels, respectively) and fed a normal or high-fat diet for 90 days. We observed high-fat diet significantly increased body mass, plasma lipoproteins and cholesterol, liver injury and hepatic triglycerides in rats and these outcomes were exacerbated by exposure to Cr(VI). Cr(VI) alone increased hepatic expression of alpha fetoprotein, a liver cancer biomarker, with evidence suggesting Cr(VI) and high-fat diet together increased these levels more than either exposure alone. Our results indicate Cr(VI) at very low levels combined with high-fat diet worsens liver disease, emphasizing the need to reconsider current Cr(VI) drinking water regulations.
慢性肝病被列为“十大死因”之一,每年导致数百万人死亡。最常见的肝病——代谢功能障碍相关脂肪性肝病(MASLD)的患病率在过去20年中翻了一番,且仍在上升。与此同时,环境化学物质暴露也在增加,成为肝病的关键风险因素。六价铬[Cr(VI)]是美国饮用水中的头号化学危害物,与肝病发病率增加有关,包括肝癌。人们对Cr(VI)如何导致肝病知之甚少,也没有研究考虑过Cr(VI)暴露与高脂饮食(一种已明确的MASLD风险因素)共同作用是否会引发肝病。因此,我们建立了一个体内模型来研究Cr(VI)和高脂饮食对MASLD的影响。将雄性Sprague Dawley大鼠暴露于饮用水中的Cr(VI)(0、0.05或0.1 mg/L,分别反映世界卫生组织和美国环境保护局的最大污染物水平),并给予正常或高脂饮食90天。我们观察到高脂饮食显著增加了大鼠的体重、血浆脂蛋白和胆固醇、肝损伤及肝甘油三酯,而Cr(VI)暴露加剧了这些结果。单独的Cr(VI)增加了肝癌生物标志物甲胎蛋白的肝脏表达,有证据表明Cr(VI)和高脂饮食共同作用使这些水平的升高幅度超过单独任何一种暴露。我们的结果表明,极低水平的Cr(VI)与高脂饮食相结合会加重肝病,这凸显了重新审视当前Cr(VI)饮用水法规的必要性。