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Query: UNIPROT:P47989 (
xanthine oxidase
)
8,633
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Oxidation of low-density lipoprotein (LDL) has been recognized as playing an important role in the development and progression of atherosclerotic heart disease. Human LDL was isolated and challenged with a range of oxidants either in the presence or absence of
AGE
or its diethyl ether extract. Oxidative modification of the LDL fraction using CuSO(4), 5-lipoxygenase and xanthine/
xanthine oxidase
was monitored by both the appearance of thiobarbituric-acid substances (TBA-RS) and an increase in electrophoretic mobility. This study indicates that
AGE
is an effective antioxidant as it scavenged superoxide ions and reduced lipid peroxide formation in cell free assays. Superoxide production was completely inhibited in the presence of a 10% (v/v) aqueous preparation of
AGE
and reduced by 34% in the presence of a 10% (v/v) diethyl ether extract of
AGE
. The presence of 10% (v/v) diethyl ether extract of
AGE
significantly reduced Cu(2+) and 15-lipoxygenase-mediated lipid peroxidation of isolated LDL by 81% and 37%, respectively. In addition, it was found that
AGE
also had the capacity to chelate copper ions. In contrast, the diethyl ether extract of
AGE
displayed no copper binding capacity, but demonstrated distinct antioxidant properties. These results support the view that
AGE
inhibits the in vitro oxidation of isolated LDL by scavenging superoxide and inhibiting the formation of lipid peroxides.
AGE
was also shown to reduce LDL oxidation by the chelation of Cu(2+). Thus,
AGE
may have a role to play in preventing the development and progression of atherosclerotic disease.
...
PMID:Antioxidant properties of aged garlic extract: an in vitro study incorporating human low density lipoprotein. 1255 47
Oxidative stress is thought to be one of the causative factors contributing to insulin resistance and type 2 diabetes. Previously, we showed that reactive oxygen species (ROS) production is significantly increased in adipocytes from high-fat diet-induced obese and insulin-resistant mice (HF). ROS production was also associated with the increased activity of PKC-delta. In the present studies, we hypothesized that PKC-delta contributes to ROS generation and determined their intracellular source. NADPH oxidase inhibitor diphenyleneiodonium chloride (DPI) reduced ROS levels by 50% in HF adipocytes, and inhibitors of NO synthase (L-NAME, 1 mM),
xanthine oxidase
(allopurinol, 100 microM),
AGE
formation (aminoguanidine, 10 microM), or the mitochondrial uncoupler (FCCP, 10 microM) had no effect. Rottlerin, a selective PKC-delta inhibitor, suppressed ROS levels by approximately 50%. However, neither GO-6976 nor LY-333531, effective inhibitors toward conventional PKC or PKC-beta, respectively, significantly altered ROS levels in HF adipocytes. Subsequently, adenoviral-mediated expression of wild-type PKC-delta or its dominant negative mutant (DN-PKC-delta) in HF adipocytes resulted in either a twofold increase in ROS levels or their suppression by 20%, respectively. In addition, both ROS levels and PKC-delta activity were sharply reduced by glucose depletion. Taken together, these results suggest that PKC-delta is responsible for elevated intracellular ROS production in HF adipocytes, and this is mediated by high glucose and NADPH oxidase.
...
PMID:PKC-delta-dependent activation of oxidative stress in adipocytes of obese and insulin-resistant mice: role for NADPH oxidase. 1550 33
