Reactive oxygen species are involved in nickel inhibition of DNA repair

✍ Scribed by S. Lynn; F. H. Yew; K. S. Chen; K. Y. Jan

• Publisher: John Wiley and Sons
• Year: 1997
• Tongue: English
• Weight: 123 KB
• Volume: 29
• Category: Article
• ISSN: 0893-6692
• DOI: 10.1002/(sici)1098-2280(1997)29:2<208::aid-em11>3.0.co;2-i

✦ Synopsis

Nickel has been shown to inhibit DNA repair in a into the DNase I-activated calf thymus DNA was way that may play a role in its toxicity. Since nickel stronger than the ligation of poly(dA)roligo(dT), treatment increases cellular reactive oxygen species whereas H 2 O 2 was more potent in inhibiting DNA (ROS), we have investigated the involvement of ligation than DNA polymerization. Nickel, in the ROS in nickel inhibition of DNA repair. Inhibition presence of H 2 O 2 , exhibited a synergistic inhibition of glutathione synthesis or catalase activity in-on both DNA polymerization and ligation and creased the enhancing effect of nickel on the cyto-caused protein fragmentation. In addition, glutathitoxicity of ultraviolet (UV) light. Inhibition of cata-one could completely recover the inhibition by lase and glutathione peroxidase activities also en-nickel or H 2 O 2 alone but only partially recover the hanced the retardation effect of nickel on the inhibition by nickel plus H 2 O 2 . Therefore, nickel rejoining of DNA strand breaks accumulated by hy-may bind to DNA-repair enzymes and generate oxdroxyurea plus cytosine-b-D-arabinofuranoside in ygen-free radicals to cause protein degradation in UV-irradiated cells. Since DNA polymerization and situ. This irreversible damage to the proteins inligation are involved in the DNA-break rejoining, volved in DNA repair, replication, recombination, we have investigated the effect of ROS on these two and transcription could be important for the toxic steps in an extract of Chinese hamster ovary cells. effects of nickel.