Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P04179 (
MnSOD
)
2,777
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
MnSOD
is the only mammalian isoform of SOD that is necessary for life.
MnSOD
(-/-) mice die soon after birth, and
MnSOD
(+/-) mice are more susceptible to oxidative stress than wild-type (WT) mice. In this study, we examined vasomotor function responses in aortas of
MnSOD
(+/-) mice under normal conditions and during oxidative stress. Under normal conditions, contractions to serotonin (
5-HT
) and prostaglandin F2alpha (PGF2alpha), relaxation to ACh, and superoxide levels were similar in aortas of WT and
MnSOD
(+/-) mice. The mitochondrial inhibitor antimycin A reduced contraction to PGF2alpha and impaired relaxation to ACh to a similar extent in aortas of WT and
MnSOD
(+/-) mice. The Cu/ZnSOD and extracellular SOD inhibitor diethyldithiocarbamate (DDC) paradoxically enhanced contraction to
5-HT
and superoxide more in aortas of WT mice than in
MnSOD
(+/-) mice. DDC impaired relaxation to ACh and reduced total SOD activity similarly in aortas of both genotypes. Tiron, a scavenger of superoxide, normalized contraction to
5-HT
, relaxation to ACh, and superoxide levels in DDC-treated aortas of WT and
MnSOD
(+/-) mice. Hypoxia, which reportedly increases superoxide, reduced contractions to
5-HT
and PGF2alpha similarly in aortas of WT and
MnSOD
(+/-) mice. The vasomotor response to acute hypoxia was similar in both genotypes. In summary, under normal conditions and during acute oxidative stress, vasomotor function is similar in WT and
MnSOD
(+/-) mice. We speculate that decreased mitochondrial superoxide production may preserve nitric oxide bioavailability during oxidative stress.
...
PMID:Vasomotor responses in MnSOD-deficient mice. 1531 74
