Redox- and non-redox metal induced formation of free radicals and their role in human disease

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F62690094%3A18470%2F16%3A50003734" target="_blank" >RIV/62690094:18470/16:50003734 - isvavai.cz</a>

Alternative codes found

RIV/62690094:18450/16:50003734 RIV/00179906:_____/16:10321970

Result on the web

<a href="http://mmsl.cz/viCMS/soubory/pdf/MMSL_2015_4_4_WWW.pdf" target="_blank" >http://mmsl.cz/viCMS/soubory/pdf/MMSL_2015_4_4_WWW.pdf</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1007/s00204-015-1579-5" target="_blank" >10.1007/s00204-015-1579-5</a>

Result language

angličtina

Original language name

Redox- and non-redox metal induced formation of free radicals and their role in human disease

Original language description

Transition metal ions are key elements of various biological processes ranging from oxygen formation to hypoxia sensing, and therefore, their homeostasis is maintained within strict limits through tightly regulated mechanisms of uptake, storage and secretion. The breakdown of metal ion homeostasis can lead to an uncontrolled formation of reactive oxygen species, ROS (via the Fenton reaction, which produces hydroxyl radicals), and reactive nitrogen species, RNS, which may cause oxidative damage to biological macromolecules such as DNA, proteins and lipids. An imbalance between the formation of free radicals and their elimination by antioxidant defense systems is termed oxidative stress. Most vulnerable to free radical attack is the cell membrane which may undergo enhanced lipid peroxidation, finally producing mutagenic and carcinogenic malondialdehyde and 4-hydroxynonenal and other exocyclic DNA adducts. While redox-active iron (Fe) and copper (Cu) undergo redox-cycling reactions, for a second group of redox-inactive metals such as arsenic (As) and cadmium (Cd), the primary route for their toxicity is depletion of glutathione and bonding to sulfhydryl groups of proteins. While arsenic is known to bind directly to critical thiols, other mechanisms, involving formation of hydrogen peroxide under physiological conditions, have been proposed. Redox-inert zinc (Zn) is the most abundant metal in the brain and an essential component of numerous proteins involved in biological defense mechanisms against oxidative stress. The depletion of zinc may enhance DNA damage by impairing DNA repair mechanisms. Intoxication of an organism by arsenic and cadmium may lead to metabolic disturbances of redox-active copper and iron, with the occurrence of oxidative stress induced by the enhanced formation of ROS/RNS.

Czech name

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Czech description

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Type

J_x - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

CEP classification

FR - Pharmacology and apothecary chemistry

OECD FORD branch

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Project

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Continuities

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2016

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

Archives of toxicology

ISSN

0340-5761

e-ISSN

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Volume of the periodical

90

Issue of the periodical within the volume

1

Country of publishing house

DE - GERMANY

Number of pages

37

Pages from-to

1-37

UT code for WoS article

000370196900001

EID of the result in the Scopus database

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