Metabolic responses and microbial community changes to long chain fatty acids: Ammonia synergetic co-inhibition effect during biomethanation.

Anaerobic co-digestion is an established strategy for increasing methane production of substrates. However, substrates rich in proteins and lipids could cause a long chain fatty acids (LCFA)-ammonia synergetic co-inhibition effect. The microbial mechanisms of this co-inhibition are still unclear. The current study explored the effect of the synergetic co-inhibition on microbial community changes and prediction of metabolic enzymes to reveal the microbial mechanisms of the co-inhibition effect. The results indicated that during the synergetic co-inhibition, methanogens were mainly affected by ammonia. Decreased relative abundances of Petrimonas (82%) and Paraclostridium (67%) showed that ammonia inhibition contributed to the suppression of LCFA ß-oxidation under the synergetic co-inhibition conditions. The accumulation of more LCFA could further suppress microorganisms' activities involved in several steps of anaerobic digestion. Finally, decrease of critical enzymes' abundances confirmed the synergetic co-inhibition effect. Overall, the current study provides novel insights for the alleviation of synergetic co-inhibition during anaerobic digestion.

Hydrogen ameliorates lung injury in a rat model of subacute exposure to concentrated ambient PM2.5 via Aryl hydrocarbon receptor.

BACKGROUND: Ambient fine particulate matter (PM2.5) could induce lung injury. Aryl hydrocarbon receptor (AhR) is involved in the molecular mechanisms of prooxidative and pro-inflammatory effect of PM2.5. Molecular hydrogen has antioxidant properties. The protective effect and mechanism of hydrogen on PM2.5-induced lung injury remain unclear. OBJECTIVES: This study aimed to determine whether hydrogen could alleviate lung injury in a rat model of subacute exposure to concentrated ambient PM2.5, and explore the mechanism related to AhR. METHODS: Male Wastar rats were exposed to either concentrated ambient particles (CAPs) (diameter: ≤2.5 µm, average concentration: 1328 ±â€¯730 µg/m3) or filtered air (FA) by nose-only inhalation (5 h/day, 5 days/week for 4 weeks). Hydrogen-treated rats inhaled 66.7% hydrogen from water electrolysis for 2 h after each exposure to CAPs or FA. RESULTS: CAPs inhalation induced lung injury, as demonstrated by pulmonary function decrease, histopathological damage, mucus hypersecretion [Periodic acid-Schiff (PAS) staining for mucins, immunohistochemistry and quantitative real-time PCR (RT-qPCR) for mucin 5AC (MUC5AC) expression], increased pro-inflammatory cytokines (TNF-α, IL-8 and IL-1ß) and oxidative damage indexes [malondialdehyde (MDA) and 8-isoprostane F2α (8-iso-PG)]. While, hydrogen inhalation significantly alleviated the damages mentioned above. In addition, low expression of AhR in lung tissues determined by Western Blot was found after CAPs exposure, whereas hydrogen inhibited AhR decline induced by CAPs. CONCLUSIONS: High concentrations of hydrogen could ameliorate pulmonary dysfunction, airway mucus hypersecretion, oxidation damage, and inflammation response in rats exposed to concentrated ambient PM2.5. Additionally, hydrogen alleviates lung injury induced by PM2.5 possibly through AhR-dependent mechanisms.