Effect of Low-Level Radiation on the Death of Male Germ Cells

Abstract

Hormetic and adaptive responses induced by low-level radiation in hematopoietic and immune systems have been observed, as shown by stimulatory effects on cell growth and resistance to subsequent radiation-induced cytogenetic damage. However, in terms of cell death by apoptosis, the effects of low-level radiation are controversial: Some studies showed decreased apoptosis in response to low-level radiation while others showed increased apoptosis. This controversy may be related to the radiation doses or dose rates and also, more importantly, to the cell types. Testes are one of the most radiosensitive organs. The loss of male germ cells after exposure to ionizing radiation has been attributed to apoptosis. In the present study, the effects of low-level radiation at doses up to 200 mGy on mouse male germ cells in terms of apoptosis and the expression of apoptosis-related proteins were examined at different times after whole-body exposure of mice to low-level radiation. In addition, the effect of pre-exposure to low-level radiation on subsequent cell death induced by high doses of radiation was examined to explore the possibility of low-level radiation-induced adaptive response. The results showed that low-level radiation in the dose range of 25-200 mGy induced significant increases in apoptosis in both spermatogonia and spermatocytes, with the maximal effect at 75 mGy. The increased apoptosis is most likely associated with Trp53 protein expression. Furthermore, 75 mGy low-level radiation given pre-irradiation led to an adaptive response of seminiferous germ cells to subsequent high-level radiation-induced apoptosis. These results suggest that low-level radiation induces increased apoptosis in male germ cells but also induces a significant adaptive response that decreases cell death after a subsequent high-dose irradiation.

Combined action of X-rays and nonylphenol on mouse sperm

“…This finding may be one of the reasons for diminished sperm count after exposure of spermatogonia. The increased apoptosis is most likely associated with increased levels of Trp53 protein [43]. As Yin et al [46] note, predominant expression of Trp53 is possible in spermatocytes of mice and in spermatogonia and spermatocytes of rats and humans.…”

“…The damage caused by radiation may result in cell death or modifications that can affect the normal functioning of organs and tissues. The loss of male germ cells after exposure to ionising radiation is mainly attributed to apoptosis [43]. Sensitivity to radiationinduced apoptosis is characteristic for different types of cells present in testes [44,45].…”

“…Sensitivity to radiationinduced apoptosis is characteristic for different types of cells present in testes [44,45]. Liu et al [43] report that low-level radiation in the dose-range of 25-200 mGy induces a significant increase in apoptosis in both spermatogonia and spermatocytes. This finding may be one of the reasons for diminished sperm count after exposure of spermatogonia.…”

A Small-Scale Anatomic Model for Testicular Radiation Dosimetry for Radionuclides Localized in the Human Testes

“…In recent years, the loss of male germ cells after exposure to ionizing radiation has been attributed to apoptosis. Liu et al demonstrated that absorbed doses of 25-200 mGy induced a significant increase in apoptosis in both spermatogonia and spermatocytes, with a maximal effect at 75 mGy (40).…”

Cryopreservation of Cattle, Pig, Inobuta Sperm and Oocyte after the Fukushima Nuclear Plant Accident

“…These different types of germ cells differ remarkably in their susceptibility to radiationinduced effects according to their level of reproductive activity [5]. The effect on reproductive organs and behaviour by chronic exposure to radionuclides is one of major concerns.…”