Abstract
ObjectiveExcess of fructose consumption is related to life-treating conditions that affected more than a third of the global population. Therefore, to identify a newer therapeutic strategy for the impact prevention of high fructose injury in age-related malfunctions of the gastric mucosa (GM) in the animal model is important.MethodsAdult and aged male rats were divided into control groups (standard diet, SD) and high fructose diet (HFD) groups; acute water immersion restraint stress (WIRS) was induced for evaluation of GM adaptive response and effects of testing the therapeutic potential of H2S-releasing compounds (H2S donors). Histological examination of gastric damage was done on hematoxylin-eosin stained slides. Cystathionine beta-synthase (CBS), Cystathionine gamma-lyase (CSE), and Thiosulfate-dithiol sulfurtransferase (TST) activities and oxidative index were assessed during exogenous administration of H2S donors: sodium hydrosulfide (NaHS) and the novel hybrid H2S-releasing aspirin (ATB-340). The results showed that HFD increased gastric damage in adult and aged rats. HFD-associated malfunction characterized by low activities of H2S key enzymes, inducing increased oxidation. Pretreatment with NaHS, ATB-340 of aged rats in the models of HFD, and WIRS attenuated gastric damage in contrast to vehicle-treated group (p < 0.05). The effect of ATB-340 was characterized by reverse oxidative index and increased CBS, CSE, and TST activities. In conclusion, H2S donors prevent GM age-related malfunctions by enhancement of CBS, CSE, and TST expression against fructose excess injury though reduction of oxidative damage.
Highlights
The World Health Organization defined relation between excess fructose consumption and accelerated aging, which could be a factor for multi-morbidity and has numerous harmful effects (Lyons et al, 2016; Bektas et al, 2018; Miller et al, 2018)
Several animal and human studies suggest that postprandial hyperglycemia related to excessive fructose consumption causes cellular and subcellular oxidative damage, and accelerates the age-related decline in cytoprotection by developing oxidative damage related to a modification in Hydrogen sulfide (H2S)-Nitric oxide (NO) cross-talk and redox homeostasis (Guan et al, 2012; Cao and Bian, 2018)
We determined the effects of H2S donors, such as Sodium hydrosulfide (NaHS) and ATB-340 on Cystathionine gamma-lyase (CSE) and Cystathionine beta-synthase (CBS) expression, which play a crucial role in H2S biogenesis, as well as Thiosulfate-dithiol sulfurtransferase (TST) expression which appears exclusively mitochondrial and has co-operative activity with mitochondrial ribosomal proteins L18 (MRPL18) and acts as a mitochondrial important factor for anti-oxidative stress functions and redox regulation, producing thiosulfate and recovering glutathione for defense cellular thiol proteins under oxidative stress (Szabo et al, 2014; Kimura, 2019)
Summary
The World Health Organization defined relation between excess fructose consumption and accelerated aging, which could be a factor for multi-morbidity and has numerous harmful effects (Lyons et al, 2016; Bektas et al, 2018; Miller et al, 2018). Hydrogen sulfide (H2S) system, the key endogenous signaling mediator that is operated by several enzymatic and nonenzymatic pathways, including catalytic activities of Cystathionine-b-synthase (CBS, EC 4.2.1.22), Cystathionine-glyase (CSE, EC 4.4.1.1) and Thiosulfate-dithiol sulfurtransferase (belong to sulfurtransferase superfamily and rhodanese family, another name—thiosulfate reductase (glutathione-depend), TST, EC 2.8.1.5) is known for more than 15-years study These key enzymes in H2S signaling operated in the cytosol (CBS, CSE) and mitochondria (CBS and TST) showed remarkable cytoprotective advances of their multifunctional abilities, as gas neurotransmitters, the mediator of vascular response, platelet adhesion, regulation of glucose metabolism, redox balance, and detoxification of intramitochondrial oxygen free radicals (Wallace et al, 2012; Fu et al, 2012; Szabo et al, 2014; Kanagy et al, 2017; Zhang et al, 2017).
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