Why h2

Hydrogen (H) is the lightest and most abundant element in the universe;

in its molecular form H2 is a colorless, odorless, tasteless non-toxic nonmetallic gas . Although hydrogen can burn at temperatures above 570˚C, at normal temperatures and partial pressures (at concentrations below 4%), it is a harmless gas that can act as a cellular antioxidant. Hydrogen was first used as a medical gas in 1888 by Pilcher. It was infused as a gas into patients’ rectums to identify colorectal perforations in order to avoid unnecessary surgery. Until recently hydrogen was thought to be physiologically inert, but in 2007 it was reported that hydrogen could ameliorate cerebral ischemia reperfusion injury and selectively reduce strong cytotoxic oxygen radicals, including hydroxyl radical (•OH) and peroxynitrite (ONOO−). This followed from experiments by Christensen and Sehested where molecular hydrogen was found to neutralize hydroxyl radicals in aqueous solutions at 20˚C .

The formation of oxygen and nitrogen radicals, as seen under conditions of oxidative stress, is thought to be an important if not an essential element contributing to the formation of a number of diseases, such as cardiovascular, rheumatic, gastrointestinal, neurodegenerative, metabolic, neoplastic and other diseases. It is also important in tissue injury and aging . In this process, free radicals, such as reactive oxygen species (ROS) and reactive nitrogen species (RNS), are generated as by-products of oxidative metabolism. When in excess over endogenous antioxidants, ROS/RNS can induce casual and cumulative oxidative damage to cellular macromolecules, eventually resulting in cellular dysfunction, cell death and in some cases, leading to the development of various diseases.

Mitochondria appear to be closely involved in oxidative stress and the aging process. They are the main intracellular source of free radical superoxide anion, as well as the initial target of oxidative damage. Under physiological conditions, low concentrations of ROS/RNS are generated indirectly by the electron transport chain in the inner mitochondrial membrane, and these ROS/RNS are normally neutralized by cellular antioxidants. However, excess ROS/RNS generated under pathological conditions cause progressive oxidative damage to mitochondrial membranes, proteins and mitochondrial DNA and eventually other cellular constituents.

Mitochondrial dysfunction caused by excess concentrations of ROS/RNS is found in essentially all chronic diseases. Cell death is an important consequence of mitochondrial dysfunction, and the demise of cells can occur via a number of pathways that are initiated in mitochondria and involve apoptosis, autophagy and necrosis.


Under normal physiological conditions ROS/RNS exist at low cell concentrations that do not cause excessive cellular damage. The levels of these potentially dangerous free radicals are kept in check by endogenous antioxidant systems that include superoxide dismutase, catalase, glutathione peroxidase and various vitamins. However, when the concentrations of ROS/RNS exceed the endogenous capacity to neutralize them, oxidative stress and cellular damage can occur. Excess production of ROS/RNS can occur due to a variety of exposures, from irradiation to chemical exposure or by physical stress.