الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 146 |  |  |
| | | from | 146 | | |
Abstract
There are about 5 billion users of mobile phones worldwide; this causes much exposure to the harmful effects of mobile phone EMFs. One of these harmful effects is testicular damage leading to infertility. But, thepathophysiological mechanisms of the damaging effect of these fields on many organs including the testes and whether this damage is reversible or not is still not well known.
In order to investigate the possible mechanism of damaging by EMFson testicular functions and the possibility of recovery, a total of 18 adult male White New Zealand rabbits, 6 months old and weighing 3.15–3.25 kgare arranged equally in 3 groups: control, exposed and recovery group. They were individually caged.
The exposed and recovery groups are exposed to mobile phones in standby position for 18 hours / day for 14 weeks. During this period, testicular functions are assessed by semen analysis weekly. After the end of the 14 weeks, hormonal assessment for testosterone, FSH & LH was done in addition to testicular weighting and histological examination of the testes were done. Plasma samples were also taken for assessment of the total antioxidant capacity and calculation of oxidative stress index. Then after the 14th week of exposure to mobile phones,the recovery group was preserved up to another 14 weeks to observe the possibility of recovery.
In the exposed group, there was significant dropin sperm countat the 6th weekand progressed until reach maximumat the 14th week. Also sperm motility was reduced at the 12thweekand became more significant at the 14th week. Sperm fast forward motility was also reduced at the 9thweekand became more significant at the 12th week. Recovery group showed decline in the sperm count during exposure then significant rise after 14 weeks allowed for recovery.
There was a decline in the serum total testosterone level of the exposed groupwhen compared with the control groupthen the level of testosterone rose again in the recovery group.There was also a decline in the serum FSH level of the exposedgroup when compared with the control groupthen the level of FSH showed slight rise in the recovery group.There was also a decline in the serum LH level of the exposed groupwhen compared with the control group then the level of LH showed significant rise in the recovery group.
There was no significant difference in testicular weight among the different groups.
The oxidative stress index (OSI) was significantly higher in exposed group than in control group.For the recovery group the values of oxidative stress index showed much reduction in theoxidative stress index when compared with exposed group.
Histological examination of the testes reveled degenerative changes in seminiferous tubules and Interstitial cells of Leydig as intercellular vacuoles,loss of the normal distribution of epithelial lining with appearance of several layers dark spermatogonia.
Conclusion:
The chronic exposure of MP-EMWs causes testicular damage by free radical formation due to ROS production. The free radicals lead to increased oxidative stress which in turn activates the caspase-3 causing apoptosis that affect the spermatogonia leading to decrease sperm count and also affect the Leydig cells leading to DROP in testosterone level leading to altered spermatogenesis. Moreover, disturbance in gonadotrophic hormones (FSH & LH) may suggest alternative mechanism that mediate the suppression of testicular functions.
Finally, negative documented efectsof MP exposure on testicular functions may be contributed by oxidative stress injury, disturbance in feedback hormonal control on testicular functions or direct destruction of testicular tissue that documented by histopathological examination..This damaging effect is reversible if a period of 9th weeks is allowed for sperm count to begin increasing in number but more periods is needed to return to their normal levels.