Ozone protective effects against PTZ-induced generalized seizures are mediated by reestablishment of cellular redox balance and A1 adenosine receptors.

Objectives: Epilepsy is a common seizure disorder affecting approximately 70 million people worldwide. Mitochondrial dysfunction and antioxidant/prooxidant imbalance are emerging as factors that contribute to epileptogenesis. As medical ozone was able to reestablish cellular redox balance and to maintain the protective effects mediated by A1 receptors (A1Rs), the aim of this work was to study ozone's effects on antioxidant/prooxidant balance and to clarify if A1Rs play a role in ozone's protective actions against pentylenetetrazole (PTZ)-induced convulsions in mice.

Ozone oxidative postconditioning ameliorates joint damage and decreases pro-inflammatory cytokine levels and oxidative stress in PG/PS-induced arthritis in rats.

Rheumatoid Arthritis (RA) is the most prevalent chronic condition present in ~1% of the adult population. Many pro-inflammatory mediators are increased in RA, including Reactive Oxygen Species such as nitric oxide NO, pro-inflammatory cytokines as tumor necrosis factor alpha (TNF-α), interleukin-1beta (IL-1β) and other molecules. Ozone oxidative postconditioning has regulatory effects on some pathological targets associated with RA.