Abstract
Oxidative stress plays a key role in numerous disease processes including chronic kidney disease (CKD). In general, oxygen metabolism leads to the formation of reactive oxygen species (ROS) dangerous to cells. Although enzymes and low-molecular-weight antioxidants protect against ROS, chronic imbalances of formation and elimination can eventually overwhelm endogenous defenses leading to deleterious consequences. In CKD, glutathione peroxidases (GSH-Px) play an important role in ROS metabolism. Plasma GSH-Px is synthesized in the kidney and requires selenium (Se) as a cofactor. Interestingly, Se and plasma GSH-Px are both significantly reduced in CKD, especially for those patients on hemodialysis. Supplementation of Se in these patients results in modest increases of GSH-Px, presumably from residual renal tissue. Kidney transplantation rapidly restores plasma GSH-Px. In this chapter, the relevance of these findings to CKD is explored with emphasis on renal disease processes and impact on attendant disorders including cancer and cardiovascular disease.
TY - JOUR
T1 - Selenium and selenium-dependent antioxidants in chronic kidney disease.
A1 - Zachara,Bronislaw A,
Y1 - 2015/01/07/
PY - 2015/4/11/entrez
PY - 2015/4/11/pubmed
PY - 2015/6/5/medline
KW - Antioxidants
KW - Chronic kidney disease
KW - Glutathione peroxidases
KW - Hemodialysis
KW - Selenium
SP - 131
EP - 51
JF - Advances in clinical chemistry
JO - Adv Clin Chem
VL - 68
N2 - Oxidative stress plays a key role in numerous disease processes including chronic kidney disease (CKD). In general, oxygen metabolism leads to the formation of reactive oxygen species (ROS) dangerous to cells. Although enzymes and low-molecular-weight antioxidants protect against ROS, chronic imbalances of formation and elimination can eventually overwhelm endogenous defenses leading to deleterious consequences. In CKD, glutathione peroxidases (GSH-Px) play an important role in ROS metabolism. Plasma GSH-Px is synthesized in the kidney and requires selenium (Se) as a cofactor. Interestingly, Se and plasma GSH-Px are both significantly reduced in CKD, especially for those patients on hemodialysis. Supplementation of Se in these patients results in modest increases of GSH-Px, presumably from residual renal tissue. Kidney transplantation rapidly restores plasma GSH-Px. In this chapter, the relevance of these findings to CKD is explored with emphasis on renal disease processes and impact on attendant disorders including cancer and cardiovascular disease.
SN - 0065-2423
UR - https://www.unboundmedicine.com/medline/citation/25858871/full_citation
L2 - https://linkinghub.elsevier.com/retrieve/pii/S0065-2423(14)00037-7
DB - PRIME
DP - Unbound Medicine
ER -
