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Expression of ROS catabolic enzymes in the medial nucleus tractus solitarii (nTS) of rats and upregulation during acute hypoxia
Author(s) -
Ostrowski Tim Daniel,
Barr Stacy L,
Dantzler Heather A,
Hasser Eileen M,
Kline David D,
Heesch Cheryl M
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.702.4
Subject(s) - gpx1 , glutathione peroxidase , superoxide dismutase , reactive oxygen species , endocrinology , hypoxia (environmental) , medicine , downregulation and upregulation , biology , catalase , chemistry , microbiology and biotechnology , biochemistry , oxidative stress , oxygen , organic chemistry , gene
Reactive oxygen species (ROS) increase in the nTS following acute hypoxia and likely contribute to hypoxia‐induced changes in cardiorespiratory function. H 2 O 2 is a diffusible signaling molecule that is inactivated by catalase (CAT) and glutathione peroxidase (GPx). Immunohistochemistry in untreated rats identified CAT throughout the nTS. In NeuN‐identified neurons, CAT was located perinuclear to a dense continuous network that extended into the cellular processes, presumably the endoplasmic reticulum. In microglia‐like cells, CAT was identified in the cytosol and membrane. CAT was not localized to GFAP‐identified astrocytes. Strong GPx‐1 staining was located primarily cytosolic in scattered neurons and in the nuclei of all identified astrocytes throughout the nTS. mRNA for the ROS inactivating enzymes superoxide dismutase (SOD) 1, SOD 2, CAT, Gpx1, and Gpx4 was expressed in tissue punches of the medial nTS of male rats exposed to 2 hr. of normoxia (21% O 2 , n = 6) or hypoxia (10% O 2 , n = 6). Only relative expression of Gpx1 was increased (P< 0.02) in the nTS of hypoxic (1.8 ± 0.3) versus normoxic rats (1.0 ± 0.1). Thus, enzymes responsible for catabolism of ROS are present in the nTS and upregulation of GPx‐1 may be an early compensatory response to a hypoxic challenge. Support: NIH Multi‐Investigator RO1 HL098602.