Protective Effects of IMOD and Cimetidine against Radiation-induced Cellular Damage
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Abstract:
Radiation damage is to a large extent caused by overproduction of reactive oxygen species (ROS). Radioprotectors are agents or substances that reduce the effects of radiation in healthy normal tissues while maintaining the sensitivity to radiation damage in tumor cells.Radioprotectors are agents or substances that reduce the effects of radiation in healthy normal tissues while maintaining the sensitivity to radiation damage in tumor cellsCimetidine was found more effective when used in vivo; this effect might be due to the augmentation of the presence of Sulphur atom in the compound which is ‎important for their scavenging activity.Recently, a new herbal-based medicine with immunomodulatory capacities, Setarud (IMOD), was introduced as an additional therapy in various inflammatory diseases and HIV infection. IMOD is a mixture of herbal extracts enriched with selenium. Selenium confers protection by inducing or activating cellular free-radical scavenging systems and by enhancing peroxide breakdown. This article suggests that nontoxic amount of IMOD and cimetidine have radioprotective properties and could reduce cytotoxic effects of radiation.
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protective effects of imod and cimetidine against radiation-induced cellular damage
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full textprotective effects of famotidine and vitamin c against radiation induced cellular damage in mouse spermatogenesis process
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full textProtective effects of famotidine and vitamin C against radiation induced cellular damage in mouse spermatogenesis process
*Corresponding author: Pِrof. Hossein Mozdarani, Department of Medical Genetics, School of Medical Sciences, Tarbiat Modares University, Tehran, Iran. Fax: +98 21 88006544 E-mail: [email protected] Background: Radioprotective effect of famotidine was previously shown on radiation induced micronuclei and chromosomal aberrations in human peripheral lymphocytes and mouse bone marrow cells; how...
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Journal title
volume 8 issue 1
pages -
publication date 2018-03-01
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