URANYL ACETATE INDUCES OXIDATIVE STRESS AND MITOCHONDRIAL MEMBRANE POTENTIAL COLLAPSE IN THE HUMAN DERMAL FIBROBLAST PRIMARY CELLS

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DARAEI BAHRAM; POURAHMAD JALAL; HAMIDI POUR NEDA; HOSSEINI MIR JAMAL; SHAKI FATEMEH; SOLEIMANI MASOUD

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Journal: Iranian Journal of Pharmaceutical Research Year:2012 | Volume:11 | Issue:2 Page(s): 495-501

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Title

URANYL ACETATE INDUCES OXIDATIVE STRESS AND MITOCHONDRIAL MEMBRANE POTENTIAL COLLAPSE IN THE HUMAN DERMAL FIBROBLAST PRIMARY CELLS

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Keywords

URANIUM

FIBROBLAST

LIPID PEROXIDATION

OXIDATIVE STRESS

Abstract

Cytotoxicity of depleted URANIUM, as a byproduct of military has been came to spotlight in recent decades. DU is known as a chemical rather than radioactive hazard and efforts to illustrating its mechanism is undergo, but the precise complete molecular mechanisms are still unclear. Recent studies showed that URANIUM induces biological changes in many different target tissues, such as the kidney, brain and skin. The aim of this study was to assess the impact of depleted URANIUM exposure at the cellular level in the human dermal FIBROBLAST primary cells. The human dermal FIBROBLAST primary cells incubated with different concentration (250-750 mM) of depleted URANIUM.Cytotoxicity and mitochondrial function in this cell lines were determined with the LDH leakage assay and the MTT test respectively. MDA levels were measured for determination of LIPID PEROXIDATION in DU treated cells. Besides glutathione depletion and apoptosis phenotype detection were also assessed to complete the mechanistic screening. Results showed that the cell viability ameliorates in concentration and time dependent manners following in 24, 48and 72 h incubation with DU. Moreover the significant increase in LIPID PEROXIDATION and significant decrease in cellular GSH recorded in DU treated human dermal FIBROBLAST primary cells suggesting the preoxidant effect of uranyl ions. Cytoprotective effects of N-acetylcysteine (NAC) and dramatic decrease of cell viability in buthionin sulfoxamid (BSO) pretreated cells indicated the possibility of a critical role for glutathione system in DU detoxification. Death pattern, in FIBROBLAST cells following DU treatment was varied from apoptosis to necrosis while the time and concentration increased.Since ROS formation is the initiation step for cell apoptosis, the present studies suggestUranyl-induced toxicity in the human dermal FIBROBLAST primary cells originated from OXIDATIVE STRESS and lead to occurrence of programmed cell death.

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APA: Copy

DARAEI, BAHRAM, POURAHMAD, JALAL, HAMIDI POUR, NEDA, HOSSEINI, MIR JAMAL, SHAKI, FATEMEH, & SOLEIMANI, MASOUD. (2012). URANYL ACETATE INDUCES OXIDATIVE STRESS AND MITOCHONDRIAL MEMBRANE POTENTIAL COLLAPSE IN THE HUMAN DERMAL FIBROBLAST PRIMARY CELLS. IRANIAN JOURNAL OF PHARMACEUTICAL RESEARCH (IJPR), 11(2), 495-501. SID. https://sid.ir/paper/287957/en

Vancouver: Copy

DARAEI BAHRAM, POURAHMAD JALAL, HAMIDI POUR NEDA, HOSSEINI MIR JAMAL, SHAKI FATEMEH, SOLEIMANI MASOUD. URANYL ACETATE INDUCES OXIDATIVE STRESS AND MITOCHONDRIAL MEMBRANE POTENTIAL COLLAPSE IN THE HUMAN DERMAL FIBROBLAST PRIMARY CELLS. IRANIAN JOURNAL OF PHARMACEUTICAL RESEARCH (IJPR)[Internet]. 2012;11(2):495-501. Available from: https://sid.ir/paper/287957/en

IEEE: Copy

BAHRAM DARAEI, JALAL POURAHMAD, NEDA HAMIDI POUR, MIR JAMAL HOSSEINI, FATEMEH SHAKI, and MASOUD SOLEIMANI, “URANYL ACETATE INDUCES OXIDATIVE STRESS AND MITOCHONDRIAL MEMBRANE POTENTIAL COLLAPSE IN THE HUMAN DERMAL FIBROBLAST PRIMARY CELLS,” IRANIAN JOURNAL OF PHARMACEUTICAL RESEARCH (IJPR), vol. 11, no. 2, pp. 495–501, 2012, [Online]. Available: https://sid.ir/paper/287957/en

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