1800 MHz mobile phone irradiation induced oxidative and nitrosative stress leads to p53 dependent Bax mediated testicular apoptosis in mice, Mus musculus. Issue 9 (10th April 2018)

• Record Type: Journal Article
• Authors: Shahin, Saba; Singh, Surya P.; Chaturvedi, Chandra M.
• Is Part Of: Journal of cellular physiology. Volume 233:Issue 9(2018:Sep.)
• Page Start: 7253
• Page End: 7267
• Publication Date: 2018-04-10
• Subjects: apoptosis -- mobile phone radiation -- nitrosative stress -- oxidative stress -- testis; Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.26558
• Languages: English
• ISSNs: 0021-9541

Abstract

Abstract : Present study was carried out to investigate the effect of long‐term mobile phone radiation exposure in different operative modes (Dialing, Receiving, and Stand‐by) on immature male mice. Three‐week old male mice were exposed to mobile phone (1800 MHz) radiation for 3 hr/day for 120 days in different operative modes. To check the changes/alteration in testicular histoarchitecture and serum testosterone level, HE staining and ELISA was performed respectively. Further, we have checked the redox status (ROS, NO, MDA level, and antioxidant enzymes: SOD, CAT, and GPx) by biochemical estimation, alteration in the expression of pro‐apoptotic proteins (p53 and Bax), active executioner caspase‐3, full length/uncleaved PARP‐1 (DNA repair enzyme), anti‐apoptotic proteins (Bcl‐2 and Bcl‐xL ) in testes by immunofluorescence and cytosolic cytochrome‐c by Western blot. Decreased seminiferous tubule diameter, sperm count, and viability along with increased germ cells apoptosis and decreased serum testosterone level, was observed in the testes of all the mobile phone exposed mice compared with control. We also observed that, mobile phone radiation exposure in all the three different operative modes alters the testicular redox status via increasing ROS, NO, and MDA level, and decreasing antioxidant enzymes levels leading to enhanced apoptosis of testicular cells by increasing the expression of pro‐apoptotic and apoptotic proteins along with decreasing the expression of anti‐apoptotic protein. On the basis of results, it is conclude that long‐term mobile phone radiation exposure induced oxidative stress leads to apoptosis of testicular cells and thus impairs testicular function. Abstract : 1800 MHz mobile phone radiation (MPR) induced oxidative and nitrosative stress cause histopathological changes in mice testes. Expression of p53, Bax, cytochrome‐c, and active caspase‐3 was up‐regulated while Bcl‐2, Bcl‐xL, pro‐caspase‐3, and PARP‐1 was down‐regulated in all the MPR exposed mice testes. Oxidative and nitrosative stress induced p53 dependent/independent Bax‐cytochrome‐c‐Caspase‐3 mediated pathway is involved.