Oxidative stress after antenatal betamethasone: Acute downregulation of glutathione peroxidase-3

Verhaeghe, Johan; Bree, Rieta Van; Herck, Erik Van

doi:10.1016/j.earlhumdev.2009.10.005

Cited by 14 publications

(10 citation statements)

References 37 publications

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“…Gene expression levels of all four oxidative stress defence enzymes were significantly lower in oligodendrocytes from MDD donors as compared to normal control donors. GPX and SOD activities are reduced by glucocorticoids (Pereira et al, 1995;McIntosh et al, 1998a, b;Schmidt et al, 2005;Verhaeghe et al, 2009;You et al, 2009) and it is conceivable that reduced GPX and SOD expression in MDD oligodendrocytes is secondary to elevated cortisol or related stress hormones widely believed to accompany depression. However, an explanation for down-regulation of GPX and SOD expression in oligodendrocytes but not astrocytes cannot be provided.…”

Section: Discussionmentioning

confidence: 99%

Shortened telomere length in white matter oligodendrocytes in major depression: potential role of oxidative stress

Szebeni

DiPeri

et al. 2014

Int. J. Neuropsychopharm.

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Telomere shortening is observed in peripheral mononuclear cells from patients with major depressive disorder (MDD). Whether this finding and its biological causes impact the health of the brain in MDD is unknown. Brain cells have differing vulnerabilities to biological mechanisms known to play a role in accelerating telomere shortening. Here, two glia cell populations (oligodendrocytes and astrocytes) known to have different vulnerabilities to a key mediator of telomere shortening, oxidative stress, were studied. The two cell populations were separately collected by laser capture micro-dissection of two white matter regions shown previously to demonstrate pathology in MDD patients. Cells were collected from brain donors with MDD at the time of death and age-matched psychiatrically normal control donors (N = 12 donor pairs). Relative telomere lengths in white matter oligodendrocytes, but not astrocytes, from both brain regions were significantly shorter for MDD donors as compared to matched control donors. Gene expression levels of telomerase reverse transcriptase were significantly lower in white matter oligodendrocytes from MDD as compared to control donors. Likewise, the gene expression of oxidative defence enzymes superoxide dismutases (SOD1 and SOD2), catalase (CAT) and glutathione peroxidase (GPX1) were significantly lower in oligodendrocytes from MDD as compared to control donors. No such gene expression changes were observed in astrocytes from MDD donors. These findings suggest that attenuated oxidative stress defence and deficient telomerase contribute to telomere shortening in oligodendrocytes in MDD, and suggest an aetiological link between telomere shortening and white matter abnormalities previously described in MDD.

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Section: Discussionmentioning

confidence: 99%

Shortened telomere length in white matter oligodendrocytes in major depression: potential role of oxidative stress

Szebeni

DiPeri

et al. 2014

Int. J. Neuropsychopharm.

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“…For instance, protein oxidation in human blood was elevated after resistance exercise [19]. Another study showed that plasma MDA levels were inversely correlated with protein carbonyls under betamethasone-induced oxidative stress condition [20]. The possible reason for this discrepancy may be related to the differences in experimental design and model used.…”

Section: Discussionmentioning

confidence: 99%

Oral Rg1 supplementation strengthens antioxidant defense system against exercise-induced oxidative stress in rat skeletal muscles

Yu¹,

Huang

Korivi³

et al. 2012

Journal of the International Society of Sports Nutrition

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BackgroundPrevious studies reported divergent results on nutraceutical actions and free radical scavenging capability of ginseng extracts. Variations in ginsenoside profile of ginseng due to different soil and cultivating season may contribute to the inconsistency. To circumvent this drawback, we assessed the effect of major ginsenoside-Rg1 (Rg1) on skeletal muscle antioxidant defense system against exhaustive exercise-induced oxidative stress.MethodsForty weight-matched rats were evenly divided into control (N = 20) and Rg1 (N = 20) groups. Rg1 was orally administered at the dose of 0.1 mg/kg bodyweight per day for 10-week. After this long-term Rg1 administration, ten rats from each group performed an exhaustive swimming, and remaining rats considered as non-exercise control. Tibialis anterior (TA) muscles were surgically collected immediately after exercise along with non-exercise rats.ResultsExhaustive exercise significantly (p<0.05) increased the lipid peroxidation of control group, as evidenced by elevated malondialdehyde (MDA) levels. The increased oxidative stress after exercise was also confirmed by decreased reduced glutathione to oxidized glutathione ratio (GSH/GSSG ratio) in control rats. However, these changes were completely eliminated in Rg1 group. Catalase (CAT) and glutathione peroxidase (GPx) activities were significantly (p<0.05) increased by Rg1 in non-exercise rats, while no significant change after exercise. Nevertheless, glutathione reductase (GR) and glutathione S-transferase (GST) activities were significantly increased after exercise in Rg1 group.ConclusionsThis study provide compelling evidences that Rg1 supplementation can strengthen antioxidant defense system in skeletal muscle and completely attenuate the membrane lipid peroxidation induced by exhaustive exercise. Our findings suggest that Rg1 can use as a nutraceutical supplement to buffer the exhaustive exercise-induced oxidative stress.

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“…In addition, it is unclear whether chorioamnionitis leads to antenatal conditioning of fetal redox systems which may affect the response to a pre- or postnatal second hit [ 29 – 31 ]. For example, modulation of fetal oxidative stress has been reported after maternal glucocorticoid administration in both experimental [ 32 , 33 ] and clinical settings [ 34 – 36 ], but it remains unclear if these effects vary depending on the presence or absence of inflammation. Moreover, inflammation can also result from oxidative stress [ 37 ], which highlights the role of oxygen toxicity as risk factor for adverse neonatal outcomes [ 31 ].…”

Section: Chorioamnionitis and Antenatal Corticosteroids—combined Effementioning

confidence: 99%

Can the preterm lung recover from perinatal stress?

2016

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After birth, adequate lung function is necessary for the successful adaptation of a preterm baby. Both prenatal and postnatal insults and therapeutic interventions have an immediate effect on lung function and gas exchange but also interfere with fetal and neonatal lung development. Prenatal insults like chorioamnionitis and prenatal interventions like maternal glucocorticosteroids interact but might also determine the preterm baby’s lung response to postnatal interventions (“second hit”) like supplementation of oxygen and drug therapy. We review current experimental and clinical findings on the influence of different perinatal factors on preterm lung development and discuss how well-established interventions in neonatal care might be adapted to attenuate postnatal lung injury.

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Oxidative stress after antenatal betamethasone: Acute downregulation of glutathione peroxidase-3

Abstract: Antenatal GC elicit a rapid suppression of the GPx3 antioxidant defense system which may contribute to a longer-lasting but also transient rise in lipid oxidative damage.

Cited by 14 publications

References 37 publications

Shortened telomere length in white matter oligodendrocytes in major depression: potential role of oxidative stress

Shortened telomere length in white matter oligodendrocytes in major depression: potential role of oxidative stress

Oral Rg1 supplementation strengthens antioxidant defense system against exercise-induced oxidative stress in rat skeletal muscles

Can the preterm lung recover from perinatal stress?

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