Hydrogen sulfide stimulates Mycobacterium tuberculosis respiration, growth and pathogenesis.

Hydrogen sulfide (HS) is involved in numerous pathophysiological processes and shares overlapping functions with CO and •NO. However, the importance of host-derived HS in microbial pathogenesis is unknown. Here we show that Mtb-infected mice deficient in the HS-producing enzyme cystathionine β-synthase (CBS) survive longer with reduced organ burden, and that pharmacological inhibition of CBS reduces Mtb bacillary load in mice.

Low-Dose Cannabidiol Is Safe but Not Effective in the Treatment for Crohn's Disease, a Randomized Controlled Trial.

Background: Cannabidiol (CBD) is an anti-inflammatory cannabinoid shown to be beneficial in a mouse model of IBD. Lacking any central effect, cannabidiol is an attractive option for treating inflammatory diseases.

Aim: To assess the effects of cannabidiol on Crohn's disease in a randomized placebo-controlled trial.

Inhalation exposure model of hydrogen sulfide (H₂S)-induced hypometabolism in the male Sprague-Dawley rat.

Hydrogen sulfide (H2S) has been accepted as a physiologically relevant cell-signaling molecule with both toxic and beneficial effects depending on its concentration in mammalian tissues. Notably, exposure to H2S in breathable air has been shown to decrease aerobic metabolism and induce a reversible hypometabolic-like state in laboratory rodent models. Herein, we describe an experimental exposure setup that can be used to define the reversible cardiovascular and metabolic physiology of rodents (rats) during H2S-induced hypometabolism and following recovery.

Redox Biology of Hydrogen Sulfide: Implications for Physiology, Pathophysiology, and Pharmacology.

Hydrogen sulfide (HS) has emerged as a critical mediator of multiple physiological processes in mammalian systems. The pathways involved in the production, consumption, and mechanism of action of HS appear to be sensitive to alterations in the cellular redox state and O tension. Indeed, the catabolism of HS through a putative oxidation pathway, the sulfide quinone oxido-reductase system, is highly dependent on O tension.

Metabolic and cardiac signaling effects of inhaled hydrogen sulfide and low oxygen in male rats.

Low concentrations of inhaled hydrogen sulfide (H(2)S) induce hypometabolism in mice. Biological effects of H(2)S in in vitro systems are augmented by lowering O(2) tension. Based on this, we hypothesized that reduced O(2) tension would increase H(2)S-mediated hypometabolism in vivo.