scholarly journals Role of Homologous Recombination in the Alpha-Particle-Induced Bystander Effect for Sister Chromatid Exchanges and Chromosomal Aberrations

2005 ◽  
Vol 164 (2) ◽  
pp. 141-147 ◽  
Author(s):  
H. Nagasawa ◽  
Y. Peng ◽  
P. F. Wilson ◽  
Y-C. Lio ◽  
D. J. Chen ◽  
...  
2002 ◽  
Vol 72 (4) ◽  
pp. 204-209 ◽  
Author(s):  
Sultan Ahmad ◽  
Afsahul Hoda ◽  
Mohammad Afzal

In earlier reports, hydrocortisone administration to human lymphocytes in culture was shown to cause chromosomal aberrations and increased sister chromatid exchanges. With a view to study the ameliorative action of some antioxidants against this effect, vitamins C and E were used separately and in combination along with hydrocortisone treatment, at different dosage and for different durations, on human lymphocyte cultures. The levels of chromosomal aberrations and sister chromatid exchanges were lowered, suggesting a protective role of vitamins against genotoxic damage. Administration of vitamins C and E combined appeared to be more effective in preventing chromosomal damage than separate administration, demonstrating the additive action of these vitamins against steroid-induced genotoxicity.


1999 ◽  
Vol 19 (7) ◽  
pp. 5166-5169 ◽  
Author(s):  
Eiichiro Sonoda ◽  
Masao S. Sasaki ◽  
Ciaran Morrison ◽  
Yuko Yamaguchi-Iwai ◽  
Minoru Takata ◽  
...  

ABSTRACT Sister chromatid exchange (SCE) frequency is a commonly used index of chromosomal stability in response to environmental or genetic mutagens. However, the mechanism generating cytologically detectable SCEs and, therefore, their prognostic value for chromosomal stability in mitotic cells remain unclear. We examined the role of the highly conserved homologous recombination (HR) pathway in SCE by measuring SCE levels in HR-defective vertebrate cells. Spontaneous and mitomycin C-induced SCE levels were significantly reduced for chicken DT40 B cells lacking the key HR genes RAD51 and RAD54but not for nonhomologous DNA end-joining (NHEJ)-defectiveKU70 −/− cells. As measured by targeted integration efficiency, reconstitution of HR activity by expression of a human RAD51 transgene restored SCE levels to normal, confirming that HR is the mechanism responsible for SCE. Our findings show that HR uses the nascent sister chromatid to repair potentially lethal DNA lesions accompanying replication, which might explain the lethality or tumorigenic potential associated with defects in HR or HR-associated proteins.


1989 ◽  
Vol 225 (1-2) ◽  
pp. 1-9 ◽  
Author(s):  
Vincent F. Garry ◽  
Richard L. Nelson ◽  
Elbert P. Whorton ◽  
John K. Wiencke

Sign in / Sign up

Export Citation Format

Share Document