The Role of Oxidative Stress in Metals Toxicity; Mitochondrial Dysfunction as a Key Player
| Autor: | Akram Ranjbar, Hassan Ghasemi, Farshad Rostampour |
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| Rok vydání: | 2014 |
| Předmět: | |
| Zdroj: | Galen Medical Journal. 3:2-13 |
| ISSN: | 2322-2379 2588-2767 |
| DOI: | 10.31661/gmj.v3i1.100 |
| Popis: | Metals can cause oxidative stress by increasing the formation of reactive oxygen species (ROS), which make antioxidants incapable of defiance against growing amounts of free radicals. Metal toxicity is related to their oxidative state and reactivity with other compounds. However, several reports about metals have been published in the recent years. Mitochondria, as a site of cellular oxygen consumption and energy production, can be a target for metals toxicity. Dysfunction of Mitochondrial oxidative phosphorylation led to the production of some metals toxicities metals through alteration in the activities of I, II, III, IV and V complexes and disruption of mitochondrial membrane. Reductions of adenosine triphosphate (ATP) synthesis or induction of its hydrolysis can impair the cellular energy production. In the present review study, the researchers have criticized reviews and some evidence about the oxidative stress as a mechanism of toxicity of metals. The metals disrupt cellular and antioxidant defense, reactive oxygen species (ROS) generation, and promote oxidative damage. The oxidative injuries induced by metals can be restored by use of antioxidants such as chelators, vitamin E and C, herbal medicine, and through increasing the antioxidants level. However, to elucidate many aspect of mechanism toxicity of metals, further studies are yet to be carried out. |
| Databáze: | OpenAIRE |
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