Ionizing radiation-induced testicular oxidative stress and apoptosis: the role of small GTPase RhoA

Yasar Aysun Manisalıgil1, Ayşegül Yurt1,2, Cemre Ural Özkan3

  • 1Medical Imaging Techniques, Vocational School of Health Science, Dokuz Eylul University, Izmir, Turkey.

Abstract

Insights

Ionizing radiation increases RhoA activity and cleaved caspase-3 expression in rat testes, suggesting RhoA contributes to radiation-induced testicular damage via oxidative stress and apoptosis.

Area of Science:

  • Molecular Biology
  • Radiation Biology
  • Toxicology

Background:

  • Ionizing radiation induces oxidative stress, apoptosis, and DNA damage in living organisms.
  • Small GTPases, including RhoA, Rac1, and Cdc42, are implicated in regulating oxidative stress and apoptosis.
  • Understanding the specific roles of these molecules is crucial for mitigating radiation's harmful effects.

Purpose of the Study:

  • To investigate the role of the RhoA molecule in testicular tissue damage.
  • To determine RhoA's involvement in oxidative stress and apoptosis induced by ionizing radiation.

Main Methods:

  • Rats were exposed to three doses of ionizing radiation (0.02, 0.1, and 5 Gy).
  • Testicular tissues and blood samples were collected at 2 hours, 24 hours, and 7 days post-irradiation.
  • RhoA and cleaved caspase-3 expression, RhoA activity, serum malondialdehyde (MDA), and superoxide dismutase (SOD) activity were analyzed.

Main Results:

  • RhoA expression and activity increased in a time-dependent manner with all radiation doses.
  • Cleaved caspase-3 expression also showed a time-dependent increase, indicating radiation-induced apoptosis.
  • Serum MDA levels rose, and SOD activity decreased post-irradiation, confirming oxidative stress.

Conclusions:

  • RhoA activation and expression correlate with radiation-induced testicular damage.
  • Findings suggest RhoA plays a role in exacerbating oxidative stress and apoptosis in testicular tissue following radiation exposure.

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