NDLI: Oxidative Stress and Biochemical Markers of Endothelial Dysfunction and Organ Damage under Conditions of Experimental Nonferrous Metal Intoxication

Content Provider	Springer Nature Link
Author	Dzugkoeva, F. S. Mozhaeva, I. V. Dzugkoev, S. G. Margieva, O. I. Tedtoeva, A. I. Otiev, M. A.
Copyright Year	2016
Abstract	Chronic nickel intoxication caused by parenteral nickel chloride administration (0.5 mg/kg of body weight) to Wistar rats led to ROS generation inducing LPO in erythrocyte membranes and homogenates of renal, liver, and myocardial tissue. Superoxide dismutase (SOD) activity was inhibited, while catalase activity and ceruloplasmin concentration increased. LPO and its products disrupted nitric oxide production and reduced its bioavailability, which led to the development of endothelial dysfunction and impaired microcirculatory hemodynamics. At the same time, damage of cytoplasmic membranes of internal organs (kidney, liver, and myocardium) was revealed, which was seen from reduced Na+, K+-ATPase activity in homogenates of these organs and increased serum activity of organ-specific (ALT, AST, and γ-glutamyl transpeptidase) and excretory (alkaline phosphatase) enzymes.
Starting Page	199
Ending Page	202
Page Count	4
File Format	PDF
ISSN	00074888
Journal	Bulletin of Experimental Biology and Medicine
Volume Number	162
Issue Number	2
e-ISSN	15738221
Language	English
Publisher	Springer US
Publisher Date	2016-12-02
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	nickel chloride nitric oxide lipid peroxidation antioxidant system endothelial dysfunction Biomedicine Internal Medicine Cell Biology Pathology Laboratory Medicine
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry, Genetics and Molecular Biology

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