Hydrogen Sulfide and Liver Health: Insights into Liver Diseases

Nguyen, Thuy T.P.; Nguyen, Phuc L.; Park, So-Hyun; Jung, Chang Hwa; Jeon, Tae-Il

doi:10.1089/ars.2023.0404

Cited by 5 publications

(1 citation statement)

References 206 publications

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“…Acidobacteriota is a bacterium that is widespread in the ecosystem and has been found to be associated with the seafloor sulfur cycle, with fewer studies on the regulatory mechanisms of the organism ( Flieder et al., 2021 ). Desulfobacterota is a Gram-negative bacterium that is metabolized in the intestinal to produce hydrogen sulfide (H 2 S), which is toxic to the intestinal epithelial apparatus and leads to gastrointestinal disorders ( Nguyen et al., 2023 ; Yang et al., 2023 ). Desulfobacterota and Acidobacteriota were found to be elevated in the CP group, which may be involved in the intestinal sulfur cycle and damage the intestinal mucosa through increased involvement with H 2 S-producing harmful bacteria.…”

Section: Discussionmentioning

confidence: 99%

Unraveling intestinal microbiota’s dominance in polycystic ovary syndrome pathogenesis over vaginal microbiota

Yu,

Li,

Yang

2024

Front. Cell. Infect. Microbiol.

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BackgroundPolycystic ovary syndrome (PCOS) is a prevalent endocrine disease in women, intricately linked to hormonal imbalances. The microbiota composition plays a pivotal role in influencing hormonal levels within the body. In this study, we utilized a murine model to investigate how intestinal and vaginal microbiota interact with hormones in the development of PCOS.MethodsTwenty female mice were randomly assigned to the normal group (N) and the model group (P), where the latter received daily subcutaneous injections of 0.1 mL DHEA (6 mg/100 g). Throughout the experiment, we evaluated the PCOS mouse model by estrus cycle, serum total testosterone (T), prolactin (PRL) and luteinizing hormone (LH) levels, and ovarian pathological morphology. The microbial composition in both intestinal content and vaginal microbiota were studied by 16S rRNA gene high-throughput sequencing.ResultsCompared with the N group, the P group showed significant increases in body weight, T, and PRL, with significant decrease in LH. Ovaries exhibited polycystic changes, and the estrous cycle was disrupted. The intestinal microbiota result shows that Chao1, ACE, Shannon and Simpson indexes were decreased, Desulfobacterota and Acidobacteriota were increased, and Muribaculaceae, Limosilactobacillus and Lactobacillus were decreased in the P group. T was significantly positively correlated with Enterorhabdus, and LH was significantly positively correlated with Lactobacillus. The analysis of vaginal microbiota revealed no significant changes in Chao1, ACE, Shannon, and Simpson indices. However, there were increased in Firmicutes, Bacteroidota, Actinobacteriota, Streptococcus, and Muribaculaceae. Particularly, Rodentibacter displayed a robust negative correlation with other components of the vaginal microbiota.ConclusionTherefore, the response of the intestinal microbiota to PCOS is more significant than that of the vaginal microbiota. The intestinal microbiota is likely involved in the development of PCOS through its participation in hormonal regulation.

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Section: Discussionmentioning

confidence: 99%

Unraveling intestinal microbiota’s dominance in polycystic ovary syndrome pathogenesis over vaginal microbiota

Yu,

Li,

Yang

2024

Front. Cell. Infect. Microbiol.

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Cystathionine γ‐lyase contributes to exacerbation of periodontal destruction in experimental periodontitis under hyperglycemia

Song,

He,

Cheng

et al. 2024

Journal of Periodontology

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BackgroundDiabetes is one of the major inflammatory comorbidities of periodontitis via 2‐way interactions. Cystathionine γ‐lyase (CTH) is a pivotal endogenous enzyme synthesizing hydrogen sulfide (H2S), and CTH/H2S is crucially implicated in modulating inflammation in various diseases. This study aimed to explore the potential role of CTH in experimental periodontitis under a hyperglycemic condition.MethodsCTH‐silenced and normal human periodontal ligament cells (hPDLCs) were cultured in a high glucose and Porphyromonas gingivalis lipopolysaccharide (P.g‐LPS) condition. The effects of CTH on hPDLCs were assessed by Cell Counting Kit 8 (CCK8), real‐time quantitative polymerase chain reaction (RT‐qPCR), and enzyme‐linked immunosorbent assay (ELISA). The model of experimental periodontitis under hyperglycemia was established on both Cth−/− and wild‐type (WT) mice, and the extent of periodontal destruction was assessed by micro‐CT, histology, RNA‐Seq, Western blot, tartrate‐resistant acid phosphatase (TRAP) staining and immunostaining.ResultsCTH mRNA expression increased in hPDLCs in response to increasing concentration of P.g‐LPS stimulation in a high glucose medium. With reference to WT mice, Cth−/− mice with experimental periodontitis under hyperglycemia exhibited reduced bone loss, decreased leukocyte infiltration and hindered osteoclast formation, along with reduced expression of proinflammatory cytokines interleukin‐6 (IL‐6) and tumor necrosis factor alpha (TNF‐α) in periodontal tissue. RNA‐seq‐enriched altered NF‐κB pathway signaling in healthy murine gingiva with experimental periodontitis mice under hyperglycemia. Accordingly, phosphorylation of p65 (P‐p65) was alleviated in CTH‐silenced hPDLCs, leading to decreased expression of IL6 and TNF. CTH knockdown inhibited activation of nuclear factor kappa‐B (NF‐κB) pathway and decreased production of proinflammatory cytokines under high glucose and P.g‐LPS treatment.ConclusionThe present findings suggest the potential of CTH as a therapeutic target for tackling periodontitis in diabetic patients.

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Chronic Exposure to Arsenic and Fluoride Starting at Gestation Alters Liver Mitochondrial Protein Expression and Induces Early Onset of Liver Fibrosis in Male Mouse Offspring

González-Alfonso,

Petrosyan,

Del Razo

et al. 2024

Biol Trace Elem Res

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The presence of arsenic (As) and fluoride (F−) in drinking water is of concern due to the enormous number of individuals exposed to this condition worldwide. Studies in cultured cells and animal models have shown that As- or F-induced hepatotoxicity is primarily associated with redox disturbance and altered mitochondrial homeostasis. To explore the hepatotoxic effects of chronic combined exposure to As and F− in drinking water, pregnant CD-1 mice were exposed to 2 mg/L As (sodium arsenite) and/or 25 mg/L F− (sodium fluoride). The male offspring continued the exposure treatment up to 30 (P30) or 90 (P90) postnatal days. GSH levels, cysteine synthesis enzyme activities, and cysteine transporter levels were investigated in liver homogenates, as well as the expression of biomarkers of ferroptosis and mitochondrial biogenesis-related proteins. Serum transaminase levels and Hematoxylin–Eosin and Masson trichrome-stained liver tissue slices were examined. Combined exposure at P30 significantly reduced GSH levels and the mitochondrial transcription factor A (TFAM) expression while increasing lipid peroxidation, free Fe 2+, p53 expression, and serum ALT activity. At P90, the upregulation of cysteine uptake and synthesis was associated with a recovery of GSH levels. Nevertheless, the downregulation of TFAM continued and was now associated with a downstream inhibition of the expression of MT-CO2 and reduced levels of mtDNA and fibrotic liver damage. Our experimental approach using human-relevant doses gives evidence of the increased risk for early liver damage associated with elevated levels of As and F− in the diet during intrauterine and postnatal period.

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Hydrogen Sulfide and Liver Health: Insights into Liver Diseases

Cited by 5 publications

References 206 publications

Unraveling intestinal microbiota’s dominance in polycystic ovary syndrome pathogenesis over vaginal microbiota

Unraveling intestinal microbiota’s dominance in polycystic ovary syndrome pathogenesis over vaginal microbiota

Cystathionine γ‐lyase contributes to exacerbation of periodontal destruction in experimental periodontitis under hyperglycemia

Chronic Exposure to Arsenic and Fluoride Starting at Gestation Alters Liver Mitochondrial Protein Expression and Induces Early Onset of Liver Fibrosis in Male Mouse Offspring

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