Endogeous sulfur dioxide protects against oleic acid-induced acute lung injury in association with inhibition of oxidative stress in rats

Abstract

The role of endogenous sulfur dioxide (SO 2 ), an efficient gasotransmitter maintaining homeostasis, in the development of acute lung injury (ALI) remains unidentified. We aimed to investigate the role of endogenous SO 2 in the pathogenesis of ALI. An oleic acid (OA)-induced ALI rat model was established. Endogenous SO 2 levels, lung injury, oxidative stress markers and apoptosis were examined. OA-induced ALI rats showed a markedly downregulated endogenous SO 2 /aspartate aminotransferase 1 (AAT1)/AAT2 pathway and severe lung injury. Chemical colorimetry assays demonstrated upregulated reactive oxygen species generation and downregulated antioxidant capacity in OA-induced ALI rats. However, SO 2 increased endogenous SO 2 levels, protected against oxidative stress and alleviated ALI. Moreover, compared with OA-treated cells, in human alveolar epithelial cells SO 2 downregulated O 2 À and OH À generation. In contrast, L-aspartic acid-b-hydroxamate (HDX, Sigma-Aldrich Corporation), an inhibitor of endogenous SO 2 generating enzyme, promoted free radical generation, upregulated poly (ADP-ribose) polymerase expression, activated caspase-3, as well as promoted cell apoptosis. Importantly, apoptosis could be inhibited by the free radical scavengers glutathione (GSH) and N-acetyl-L-cysteine (NAC). The results suggest that SO 2 /AAT1/AAT2 pathway might protect against the development of OA-induced ALI by inhibiting oxidative stress.

Catalase as a sulfide-sulfur oxido-reductase: An ancient (and modern?) regulator of reactive sulfur species (RSS)

“…SO 2 is also endogenously generated in vertebrate tissues including the vasculature and its production appears to be physiologically regulated [54], [55], [56], [57]. Like H 2 S, SO 2 is toxic in excess [58], [59], but at lower concentrations it vasodilates arteries and protects tissues against ischemic conditions, reperfusion injury and oxidative stress [57], [60], [61], [62], [63], [64], [65], [66], [67]. SO 2 is reportedly rapidly hydrated in the lung and with a pKa of ~9 form sulfite (SO 3 -2 ) and bisulfite (HSO 3 -1 ) in a 3:1 Molar ratio [68].…”

Apigenin Attenuates β-Receptor-Stimulated Myocardial Injury Via Safeguarding Cardiac Functions and Escalation of Antioxidant Defence System

“…Apigenin (AP) (4, 5,7-trihydroxyflavone) is a flavonoid copious in apples, celery oranges and wheat sprouts [26][27][28]. It has been confirmed to help on the road to recovery of cardiovascular circumstances, thought-provoking immune system, inhibiting platelet aggregation, anti-inflammatory activity and providing some shield against cancer [29][30][31][32]. An assortment of enzymatic and non-enzymatic causes of reactive oxygen species (ROS) exists in blood vessels.…”

Gold nanostars mediated combined photothermal and photodynamic therapy and X-ray imaging for cancer theranostic applications

“…The decreased GSH level is conducive to cell apoptosis. 34 As shown in Figure 7(C), apoptosis level of the GNSTs with NIR irradiation treatment group significantly increased to 50.3 AE 2.8% (p < 0.05), which was inversely associated with GSH level of the same group. However, when NaN 3 existed, the apoptosis level decreased to 37.7 AE 1.9%, suggesting that the apoptosis of GNSTs with NIR irradiation treatment group may be caused by ROS as well as heat.…”