Ameliorative role of some antioxidants against sub chronic copper toxicity in rats.

Research Abstract

The rapid growth of nanotechnology suggests that it will soon find wide application in daily consumer products and new pharmaceutical, electronic, and other industries. However, to date, there is still a lack of information regarding the human health and environmental implications of manufactured nanomaterials. Copper nanoparticles (nano-copper) have shown great promise as osteoporosis-treatment drugs, antibacterial materials, additives in livestock and poultry feed, and intrauterine contraceptive devices. Furthermore, nano-copper has been widely used in industry, e.g., as an additive in lubricants, for metallic coating, and as a highly reactive catalyst in organic hydrogen reactions. Usually, a variation in the size of metal nanoparticles results in bare nanoparticles possessing excessive surface energy, and this leads to an alteration in their catalytic properties. It is established that copper nanoparticles distribute in organs and tissues of animals and cause specific structural changes. The increase of copper nanoparticles in organism up to toxical threshold (maximum tolerated dose) results in dystrophy and tissue necrosis. Oxidative stress represents an imbalance between the production and manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage. Disturbances in the normal redox state of tissues can cause toxic effects through the production of peroxides and free radicals that damage all components of the cell, including proteins, lipids, and DNA. Some reactive oxidative species can even act as messengers through a phenomenon called redox signaling. A particularly destructive aspect of oxidative stress is the production of reactive oxygen species, which include free radicals and peroxides. Some of the less reactive of these species (such as superoxide) can be converted by oxidoreduction reactions with transition metals or other redox cycling compounds (including quinones) into more aggressive radical species that can cause extensive cellular damage . The major portion of long term effects is inflicted by damage on DNA. Most of these oxygen-derived species are produced at a low level by normal aerobic metabolism and the damage they cause to cells is constantly repaired. However, under the severe levels of oxidative stress that cause necrosis, the damage causes ATP depletion, preventing controlled apoptotic death and causing the cell to simply fall apart .

Research Keywords

Ameliorative role of some antioxidants against sub chronic copper toxicity in rats.