دورية أكاديمية
أعرض في EDS

In vivo chronic exposure to inorganic mercury worsens hypercholesterolemia, oxidative stress and atherosclerosis in the LDL receptor knockout mice.

التفاصيل البيبلوغرافية
العنوان: In vivo chronic exposure to inorganic mercury worsens hypercholesterolemia, oxidative stress and atherosclerosis in the LDL receptor knockout mice.
المؤلفون: Queiroz MIC; Institute of Chemistry and Biotecnology, Federal University do Alagoas (UFAL), AL, Brazil., Lazaro CM; Dept of Structural and Functional Biology, Biology Institute, State University of Campinas (Unicamp), SP, Brazil., Dos Santos LMB; Dept of Structural and Functional Biology, Biology Institute, State University of Campinas (Unicamp), SP, Brazil., Rentz T; Dept of Structural and Functional Biology, Biology Institute, State University of Campinas (Unicamp), SP, Brazil., Virgilio-da-Silva JV; Dept Genetics and Evolution, Microbiology and Immunology, Biology Institute, State University of Campinas (Unicamp), SP, Brazil., Moraes-Vieira PMM; Dept Genetics and Evolution, Microbiology and Immunology, Biology Institute, State University of Campinas (Unicamp), SP, Brazil., Cunha FAS; Institute of Chemistry and Biotecnology, Federal University do Alagoas (UFAL), AL, Brazil; Institute of Chemistry, Federal University of Bahia (UFBA), Salvador, BA, Brazil., Santos JCC; Institute of Chemistry and Biotecnology, Federal University do Alagoas (UFAL), AL, Brazil., Vercesi AE; Dept of Pathology, Faculty of Medical Sciences, State University of Campinas (Unicamp), SP, Brazil., Leite ACR; Institute of Chemistry and Biotecnology, Federal University do Alagoas (UFAL), AL, Brazil. Electronic address: ana.leite@iqb.ufal.br., Oliveira HCF; Dept of Structural and Functional Biology, Biology Institute, State University of Campinas (Unicamp), SP, Brazil. Electronic address: ho98@unicamp.br.
المصدر: Ecotoxicology and environmental safety [Ecotoxicol Environ Saf] 2024 Apr 15; Vol. 275, pp. 116254. Date of Electronic Publication: 2024 Mar 27.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Elsevier Country of Publication: Netherlands NLM ID: 7805381 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1090-2414 (Electronic) Linking ISSN: 01476513 NLM ISO Abbreviation: Ecotoxicol Environ Saf Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Amsterdam, Netherlands : Elsevier
مواضيع طبية MeSH: Atherosclerosis*/chemically induced , Hypercholesterolemia* , Mercury*/toxicity, Animals ; Mice ; Hydrogen Peroxide ; Kidney Diseases ; Mice, Knockout ; Oxidative Stress/physiology ; Receptors, LDL/genetics
مستخلص: Heavy metal exposure leads to multiple system dysfunctions. The mechanisms are likely multifactorial and involve inflammation and oxidative stress. The aim of this study was to evaluate markers and risk factors for atherosclerosis in the LDL receptor knockout mouse model chronically exposed to inorganic mercury (Hg) in the drinking water. Results revealed that Hg exposed mice present increased plasma levels of cholesterol, without alterations in glucose. As a major source and target of oxidants, we evaluated mitochondrial function. We found that liver mitochondria from Hg treated mice show worse respiratory control, lower oxidative phosphorylation efficiency and increased H 2 O 2 release. In addition, Hg induced mitochondrial membrane permeability transition. Erythrocytes from Hg treated mice showed a 50% reduction in their ability to take up oxygen, lower levels of reduced glutathione (GSH) and of antioxidant enzymes (SOD, catalase and GPx). The Hg treatment disturbed immune system cells counting and function. While lymphocytes were reduced, monocytes, eosinophils and neutrophils were increased. Peritoneal macrophages from Hg treated mice showed increased phagocytic activity. Hg exposed mice tissues present metal impregnation and parenchymal architecture alterations. In agreement, increased systemic markers of liver and kidney dysfunction were observed. Plasma, liver and kidney oxidative damage indicators (MDA and carbonyl) were increased while GSH and thiol groups were diminished by Hg exposure. Importantly, atherosclerotic lesion size in the aorta root of Hg exposed mice were larger than in controls. In conclusion, in vivo chronic exposure to Hg worsens the hypercholesterolemia, impairs mitochondrial bioenergetics and redox function, alters immune cells profile and function, causes several tissues oxidative damage and accelerates atherosclerosis development.
Competing Interests: Declaration of Competing Interest All authors have no financial and personal relationships with other people or organizations that could inappropriately influence this work. The data that support the findings of this study are available from the corresponding author upon reasonable request.
(Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)
فهرسة مساهمة: Keywords: Atherosclerosis; Hypercholesterolemia; Macrophage; Mercury toxicity; Mitochondria; Oxidative stress
المشرفين على المادة: BBX060AN9V (Hydrogen Peroxide)
FXS1BY2PGL (Mercury)
0 (Receptors, LDL)
تواريخ الأحداث: Date Created: 20240328 Date Completed: 20240412 Latest Revision: 20240425
رمز التحديث: 20240425
DOI: 10.1016/j.ecoenv.2024.116254
PMID: 38547729
قاعدة البيانات: MEDLINE
الوصف
تدمد:1090-2414
DOI:10.1016/j.ecoenv.2024.116254