**3. Ways in which free radicals form in the cell**

Common biochemical events, such as those which occur during normal respiration, cause reduction–oxidation (redox) reactions. The molecular oxygen in mitochondria is gradually diminished with the adding of four electrons to form water. Several toxic intermediate derivatives occur during this event. These include superoxide radicals (O−2), hydrogen peroxide (H2O2) and hydroxyl (OH− ). In addition, some intracellular oxidases such as xanthine oxidase directly form superoxide radicals as a result of their activities. It catalyzes the formation of free radicals (Fe+++ H2O2 → Fe++++ OH− + OH− ) as in the Fenton reaction by exchanging free electrons during some intracellular reactions in exchange metals such as copper and iron. To play a part in the Fenton reaction, the intracellular free iron, occuring in the ferric state (Fe+++), must initially be reduced to its ferrous (Fe++) form. Iron and superoxide are both required for maximum oxidative cell damage as the reduction is amplified by the superoxide ion.

By absorption of radiant energy (such as ultraviolet light, X-rays): For example, water can be hydrolyzed to hydroxyl (OH<sup>−</sup> ) and hydrogen (H+ ) free radicals with ionizing radiation.

By the intracellular enzymatic metabolism of external chemicals or drugs: For example, CCl3 free radical is formed as a result of the intracellular metabolism of carbon tetrachloride (CCl4).

Nitric oxide (NO), an important chemical mediator normally synthesized in various cell types, reacts with oxygen, especially non-radical peroxynitrite, a type of free oxygen that inhibits mitochondrial respiration, as well as the radical nitrogen dioxide (NO2) and nitrogen trioxide (NO3) [1]. Common free radicals, their symbols and identities are shown in the table below (**Table 1**):

