Anti-inflammatory properties of molecular hydrogen: investigation on parasite-induced liver inflammation

Abstract

Molecular hydrogen reacts with the hydroxyl radical, a highly cytotoxic species produced in inflamed tissues. It has been suggested therefore to use gaseous hydrogen in a new anti-inflammatory strategy. We tested this idea, with the aid of the equipment and skills of COMEX SA in Marseille, a group who experiments with oxygen–hydrogen breathing mixtures for professional deep-sea diving. The model used was schistosomiasis-associated chronic liver inflammation. Infected animals stayed 2 weeks in an hyperbaric chamber in a normal atmosphere supplemented with 0.7 MPa hydrogen. The treatment had significant protective effects towards liver injury, namely decreased fibrosis, improvement of hemodynamics, increased NOSII activity, increased antioxidant enzyme activity, decreased lipid peroxide levels and decreased circulating TNF-α levels. Under the same conditions, helium exerted also some protective effects, indicating that hydroxyl radical scavenging is not the only protective mechanism. These findings indicate that the proposed anti-inflammatory strategy deserves further attention. © 2001 Académie des sciences/Éditions scientifiques et médicales Elsevier SAS inflammation / molecular hydrogen / hydroxyl radical / hyperbaric medicine

Study details

Article type

Original Research

Disease / injury model

Schistosoma mansoni-induced chronic liver inflammation (schistosomiasis)

Duration

2 weeks

Dose comparison

Only one hydrogen concentration (0.7 MPa) was used; no dose comparison performed.

Dose-dependent effect

No

Outcome

Positive

Findings

Hyperbaric molecular hydrogen treatment significantly reduced parasite-induced liver inflammation in mice, as evidenced by decreased liver fibrosis, improved hemodynamics, increased NOSII and antioxidant enzyme activities, decreased lipid peroxides, and reduced circulating TNF-α. Helium also had some protective effects, but to a lesser extent, suggesting additional mechanisms beyond hydroxyl radical scavenging.