Hypoxia inhibits semicarbazide-sensitive amine oxidase activity in adipocytes

Repessé, Xavier; Moldes, Marthe; Muscat, Adeline; Vatier, Camille; Chétrite, G.; Gille, Thomas; Planès, Carole; Filip, Anna; Mercier, Nathalie; Duranteau, Jacques; Fève, Bruno

doi:10.1016/j.mce.2015.04.011

Cited by 8 publications

(5 citation statements)

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“…Pargyline (1 μM) was used to specifically inhibit MAO-B (K i 0.5 μM) and a higher concentration (10 μM) was used to inhibit both MAO-A and B (K i for pargyline at MAO-A = 15 μM Fowler et al, 1982 ). Semicarbazide was used to specifically inhibit SSAO, at a concentration (1 mM) routinely used in monoamine assays to selectively inhibit SSAO activity (K i 15 μM Lizcano et al, 1996 ; Repessé et al, 2015 ). Oxidase activity was quantified as the amount of H 2 O 2 produced per minute normalized to the amount of protein.…”

Section: Resultsmentioning

confidence: 99%

Perivascular Adipose Tissue's Impact on Norepinephrine-Induced Contraction of Mesenteric Resistance Arteries

Ayala‐Lopez¹,

Thompson²,

Watts³

2017

Front. Physiol.

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Background: Perivascular adipose tissue (PVAT) can decrease vascular contraction to NE. We tested the hypothesis that metabolism and/or uptake of vasoactive amines by mesenteric PVAT (MPVAT) could affect NE-induced contraction of the mesenteric resistance arteries.Methods: Mesenteric resistance vessels (MRV) and MPVAT from male Sprague-Dawley rats were used. RT-PCR and Western blots were performed to detect amine metabolizing enzymes. The Amplex® Red Assay was used to quantify oxidase activity by detecting the oxidase reaction product H2O2 and the contribution of PVAT on the mesenteric arteries' contraction to NE was measured by myography.Results: Semicarbazide sensitive amine oxidase (SSAO) and monoamine oxidase A (MAO-A) were detected in MRV and MPVAT by Western blot. Addition of the amine oxidase substrates tyramine or benzylamine (1 mM) resulted in higher amine oxidase activity in the MRV, MPVAT, MPVAT's adipocyte fraction (AF), and the stromal vascular fraction (SVF). Inhibiting SSAO with semicarbazide (1 mM) decreased amine oxidase activity in the MPVAT and AF. Benzylamine-driven, but not tyramine-driven, oxidase activity in the MRV was reduced by semicarbazide. By contrast, no reduction in oxidase activity in all sample types was observed with use of the monoamine oxidase inhibitors clorgyline (1 μM) or pargyline (1 μM). Inhibition of MAO-A/B or SSAO individually did not alter contraction to NE. However, inhibition of both MAO and SSAO increased the potency of NE at mesenteric arteries with PVAT. Addition of MAO and SSAO inhibitors along with the H2O2 scavenger catalase reduced PVAT's anti-contractile effect to NE. Inhibition of the norepinephrine transporter (NET) with nisoxetine also reduced PVAT's anti-contractile effect to NE.Conclusions: PVAT's uptake and metabolism of NE may contribute to the anti-contractile effect of PVAT. MPVAT and adipocytes within MPVAT are a source of SSAO.

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Section: Resultsmentioning

confidence: 99%

Perivascular Adipose Tissue's Impact on Norepinephrine-Induced Contraction of Mesenteric Resistance Arteries

Ayala‐Lopez¹,

Thompson²,

Watts³

2017

Front. Physiol.

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“…10 However, there was no significant change in the SSAO activity in the brain, which may relate to the location of SSAO and the duration of hypoxia. The activity of SSAO is different in diverse cell types after hypoxia, 32,33 which also shows a time-dependent mode, as it increased in 6 h and decreased after 24 h hypoxia. 11 Consistently, our cellular experiment showed that the activity of SSAO was gradually increased and peaked at 8 h. In addition, the hypothalamic-pituitary-adrenal (HPA) axis is activated in hypoxic conditions, 34 and then triggered methylamine release and FA formation.…”

Section: Nano-packed Coenzyme Q10 Prevented Neuronal Ferroptosis Unde...mentioning

confidence: 99%

Acute high‐altitude hypoxia exposure causes neurological deficits via formaldehyde accumulation

et al. 2022

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Acute high-altitude hypoxia exposure causes multiple adverse neurological consequences, including paralysis, blindness, sleep disturbance, mental disorder, and cognitive impairment. 1 Intellectual abilities such as concentration, perception, executive function, learning, and memory can be impaired, 2 which are caused by neuronal damage due to oxidative stress, inflammation, and other mechanisms. 3 However, the exact cellular and molecular mechanism of neurological dysfunction remains unclear. Therefore, there are no

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“…Semicarbazide-sensitive amine oxidase (SSAO), an enzyme highly expressed on adipocyte plasma membranes, converts primary amines into aldehydes, ammonium and hydrogen peroxide, and is likely involved in endothelial damage during the course of diabetes and obesity. Hypoxia-induced down-regulation of SSAO activity could represent an adaptive mechanism to lower toxic molecules production, and may thus protect from tissue injury during these harmful conditions [22]. Cytochrome oxidase (COX) dysfunction is associated with mitochondrial oxidative stress.…”

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confidence: 99%

Inflammation and Oxidative Stress: Critical Role for Metabolic Syndrome

Khaybullina¹

2017

Vasc Med Surg

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Hypoxia inhibits semicarbazide-sensitive amine oxidase activity in adipocytes

Cited by 8 publications

References 50 publications

Perivascular Adipose Tissue's Impact on Norepinephrine-Induced Contraction of Mesenteric Resistance Arteries

Perivascular Adipose Tissue's Impact on Norepinephrine-Induced Contraction of Mesenteric Resistance Arteries

Acute high‐altitude hypoxia exposure causes neurological deficits via formaldehyde accumulation

Inflammation and Oxidative Stress: Critical Role for Metabolic Syndrome

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