Induction of antioxidant enzymes by dexamethasone in the adult rat lung

José, Hicks Juan; Berenice, Silva-Gómez Adriana; Vilar-Rojas, C

doi:10.1016/s0024-3205(97)00193-8

Cited by 31 publications

(16 citation statements)

References 20 publications

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“…Interestingly, with exception of the liver of young animals, we did not observe changes in GPx activity under acute heat exposure as well. The lack of alteration of the GPx activity in aged heat-exposed rats may also be a consequence of changes in glucocorticoid hormones (Jose et al, 1997), whose level is highly affected during acute stress (Michel et al, 2007). This assumption was further corroborated by our findings for down-regulating effect of heat exposure on the GR activity in the liver of adult heat-exposed animals, since the expression of this enzyme is known to be inhibited by increase of H 2 O 2 (Gutierrez-Correa…”

Section: Discussionsupporting

confidence: 78%

l-2-oxothiazolidine-4-carboxylate influence on age- and heat exposure-dependent peroxidation in rat's liver and kidney

Hadzi‐Petrushev

Јankulovski

Milev

et al. 2012

Journal of Thermal Biology

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Section: Discussionsupporting

confidence: 78%

l-2-oxothiazolidine-4-carboxylate influence on age- and heat exposure-dependent peroxidation in rat's liver and kidney

Hadzi‐Petrushev

Јankulovski

Milev

et al. 2012

Journal of Thermal Biology

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“…In addition, FBS contains fatty acids, insulin, insulin-like growth factor (IGF) and other cytokines, all of which are involved in regulation of adipocyte differentiation. Interestingly, dexamethasone has been shown to induce Nrf2 downstream genes, including CAT, glutathione peroxidase and superoxide dismutase [47], suggesting dexamethasone is one of the key components to activate Nrf2 during adipogenesis. Insulin/IGF1 are active stimulators of NADPH-dependent ROS generation [48, 49], and can directly regulate SKN-1, a worm homolog of Nrf2 [50].…”

Section: Discussionmentioning

confidence: 99%

Nuclear factor erythroid-derived factor 2-related factor 2 regulates transcription of CCAAT/enhancer-binding protein β during adipogenesis

Hou

Xue

Bai

et al. 2012

Free Radical Biology and Medicine

119

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Nuclear factor erythroid-derived factor 2-related factor 2 (Nrf2) is a cap-n-collar basic leucine zipper transcription factor that is involved in the cellular adaptive response to oxidative stress. Our previous study reported that targeted disruption of the Nrf2 gene in mice decreases adipose tissue mass and protects against obesity induced by a high-fat diet. Deficiency of Nrf2 in preadipocytes and mouse embryonic fibroblasts led to impaired adipogenesis. Consistent with these findings, the current study found that lack of Nrf2 in primary cultured mouse preadipocytes and 3T3-L1 cells hampered adipogenic differentiation induced by hormonal cocktails. Stable knockdown of Nrf2 in 3T3-L1 cells blocked the enhanced adipogenesis caused by deficiency of kelch-like ECH-associated protein 1 (Keap1), a Cul3-adapter protein that allows for Nrf2 to be ubiquinated and degraded by the 26S protesome complex. In addition, increased production of reactive oxygen species (ROS) and activation of Nrf2 occurred at the very early stage upon adipogenic hormonal challenge in 3T3-L1 cells, followed by an immediate induction of CCAAT/enhancer-binding protein β (C/EBPβ). Knockdown of Nrf2 led to reduced expression of C/EBPβ induced by adipogenic hormonal cocktails, chemical Nrf2 activators or Keap1 silencing. Cebpβ promoter-driven reporter assays and chromatin immunoprecipitation suggested that Nrf2 associates with a consensus antioxidant response element (ARE) binding site in the promoter of the Cebpβ gene during adipogenesis and upregulates its expression. These findings demonstrate a novel role of Nrf2 beyond xenobiotic detoxification and antioxidant response, and suggest that Nrf2 is one of the transcription factors that control the early events of adipogenesis by regulating expression of Cebpβ.

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“…Recently, Ozmen (2005) reported that catalase activities were found to be significantly lower than in the control, whereas glutathione peroxidase activity was significantly increased in the erythrocytes of rats receiving the drug; glutathione reductase activity was unaffected. Studies undertaken to investigate the effect of glucocorticoids on oxidative stress and antioxidant enzymes that used different tissues have reported conflicting results (Jose et al, 1997;Pereira et al, 1995). This may be due to the specific effects exerted by glucocorticoids in different tissues.…”

Section: Discussionmentioning

confidence: 99%

Oxidative status of DBA/1J mice with type II collagen‐induced arthritis

Choi

2007

J of Applied Toxicology

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The present study was undertaken to compare the oxidant statuses of mice with collagen-induced arthritis (CIA) and those of healthy mice. For this purpose, serum oxidant products and arthritic profiles were measured in DBA/1J mice with CIA. In addition, the levels of oxidation products and the activities of antioxidant enzymes were determined in liver, heart, spleen, kidney, lung and brain. The induction of arthritis significantly increased anti-collagen antibody, rheumatoid factor, interleukin (IL)-1beta, IL-6, protein carbonyl (PCO), advanced glycation end-products (AGE), malondialdehyde (MDA) and low density lipoprotein (LDL)-cholesterol levels in serum (P < 0.05). CIA in DBA/1J mice was associated with significantly lower activities of superoxide dismutase, glutathione peroxidase and glutathione reductase in spleen but higher levels of oxidation products in spleen, kidney and liver than healthy normal mice (P < 0.05). However, lower concentrations of oxidized protein and higher activities of antioxidant enzymes were observed in CIA mouse lung and brain than in healthy normal mice. Dexamethasone treated CIA mice had decreased arthritis-related indices and showed: reduced PCO and AGE in spleen and brain, and increased PCO and AGE in heart, kidney and lung; increased MDA in heart, spleen, lung and brain; reduced SOD and GR activities in lung and brain; increased GPx activity in spleen and brain; and increased GR activity heart and spleen. These data suggest that mice with CIA were more susceptible to oxidative damage in the spleen and liver under the chronic inflammatory conditions.

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Induction of antioxidant enzymes by dexamethasone in the adult rat lung

Cited by 31 publications

References 20 publications

l-2-oxothiazolidine-4-carboxylate influence on age- and heat exposure-dependent peroxidation in rat's liver and kidney

l-2-oxothiazolidine-4-carboxylate influence on age- and heat exposure-dependent peroxidation in rat's liver and kidney

Nuclear factor erythroid-derived factor 2-related factor 2 regulates transcription of CCAAT/enhancer-binding protein β during adipogenesis

Oxidative status of DBA/1J mice with type II collagen‐induced arthritis

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