Hydrogen sulfide inhibits oxidative stress in lungs from allergic mice in vivo

Abstract

Recent studies show that endogenous hydrogen sulfide (H(2)S) plays an anti-inflammatory role in the pathogenesis of airway inflammation. This study investigated whether exogenous H(2)S may counteract oxidative stress-mediated lung damage in allergic mice. Female BALB/c mice previously sensitized with ovalbumin (OVA) were treated with sodium hydrosulfide (NaHS) 30 min before OVA challenge. Forty eight hours after antigen-challenge, the mice were killed and leukocyte counting as well as nitrite plus nitrate concentrations were determined in the bronchoalveolar lavage fluid, and lung tissue was analysed for nitric oxide synthase (NOS) activity, iNOS expression, superoxide dismutase (SOD), catalase, glutathione reductase (GR) and glutathione peroxidase (GPx) activities, thiobarbituric acid reactive species and 3-nitrotyrosine containing proteins (3-NT). Pre-treatment of OVA-sensitized mice with NaHS resulted in significant reduction of both eosinophil and neutrophil migration to the lungs, and prevented the elevation of iNOS expression and activity observed in the lungs from the untreated allergic mice, although it did not affect 3-NT. NaHS treatment also abolished the increased lipid peroxidation present in the allergic mouse lungs and increased SOD, GPx and GR enzyme activities. These results show, for the first time, that the beneficial in vivo effects of the H(2)S-donor NaHS on allergic airway inflammation involve its inhibitory action on leukocyte recruitment and the prevention of lung damage by increasing endogenous antioxidant defenses. Thus, exogenous administration of H(2)S donors may be beneficial in reducing the deleterius impact of allergic pulmonary disease, and might represent an additional class of pharmacological agents for treatment of chronic pulmonary diseases.

Oxidative stress in severe pulmonary trauma in critical ill patients. Antioxidant therapy in patients with multiple trauma — a review

“…Benetti et al [88] demonstrates that through the administration of the sodium mono-hydrogen-sulphate (NaHS) that generates sulphureted hydrogen, the accumulation of neutrophils and of eosinophils is inhibited.…”

“…In many scientific papers the beneficial effect of the sulphureted hydrogen on the inflammated lung is presented [88,[93][94][95][96][97]. Benetti et al [88] demonstrates that through the administration of the sodium mono-hydrogen-sulphate (NaHS) that generates sulphureted hydrogen, the accumulation of neutrophils and of eosinophils is inhibited.…”

“…[88][89][90]. The cellular membrane is protected by the attack of the oxidative stress by ubiquinone, which can be found in high quantities in the Golgi mechanism and in the liposomal membranes [91,92].…”

Protective effects of exogenous and endogenous hydrogen sulfide in mast cell-mediated pruritus and cutaneous acute inflammation in mice

“…Interestingly, over the last ten years, hydrogen sulfide (H2S) a new mediator that belongs to the class of endogenous gases such as nitric oxide (NO) and carbon monoxide (CO), has emerged and brought about divergent findings regarding its role in acute / chronic inflammatory responses and nociception [16][17][18][19]. However, the use of slow-releasing H2S donors (such as SG-1002, diallyl trisulfide and GYY4137) and hybrid H2S-releasing non steroidal anti-inflammatory compounds (such as the naproxen derivative strengthens the beneficial therapeutical effects of H2S in articular inflammation [20], colorectal cancer [21], periodontitis [22] and pain [23] with additional gastrointestinal safety [24].…”

GYY4137, a Novel Water-Soluble, H2S-Releasing Molecule

“…Recently, it has been hypothesized that H 2 S plays a fundamental role in the aging process (Zhang et al, 2013). Evidence that H 2 S plays a role in this process stems from a number of observations notably, that H 2 S can inhibit oxidative stress (Benetti et al, 2013;Whiteman et al, 2004), increase longevity in some model organisms (Miller & Roth, 2007) and promote the induction of genes associated with longevity (Lee, Kennedy, Tolonen, & Ruvkun, 2003;Qabazard et al, 2014). H 2 S also reduces cell senescence and promotes cellular cytoprotective systems (Predmore, Alendy, Ahmed, Leeuwenburgh, & Julian, 2010).…”