Dys-synchronous regulation of XPC and XPA in trigeminal ganglion neurons following cisplatin treatment cycles.
BACKGROUND
Cancer cells may survive cisdiamminedichloroplatinum-II (cisplatin) DNA damage through synchronous mobilization of DNA repair proteins such as xeroderma pigmentosum C and A (XPC and XPA). However, non-cancerous neuronal cells exhibit hyper-vulnerability to cisplatin which is manifest as peripheral neurotoxicity. The purpose of the present study was to evaluate the effect of cisplatin on the immunolocalization of XPC and XPA in the trigeminal ganglion.


METHODS
Fischer344 rats were treated with two cycles of cisplatin (2 mg/kg/day, i.p.) and tissues were harvested for immunohistochemistry after each treatment cycle.


RESULTS
XPA immunoreactivity was evident after each treatment cycle, however, XPC immunoreactivity was suppressed following the second treatment cycle.


CONCLUSIONS
The hyper-vulnerability of peripheral neurons to cisplatin chemotherapy may relate to the dys-synchronous regulation of XPC and XPA.
Guthrie
Oneil W
OW
Department of Communication Science and Disorders, University of Pittsburgh, Pittsburgh, PA 15260, USA. owg@duke.edu
D000818:Animals; D002945:Cisplatin / Q000494:pharmacology*; D004268:DNA-Binding Proteins / Q000096:biosynthesis*; D007150:Immunohistochemistry; D051381:Rats; D011916:Rats, Inbred F344; D011984:Sensory Receptor Cells / Q000187:drug effects* / Q000378:metabolism; D012668:Trigeminal Ganglion / Q000187:drug effects* / Q000378:metabolism; D051760:Xeroderma Pigmentosum Group A Protein / Q000096:biosynthesis*
D004268:DNA-Binding Proteins; C497314:XPA protein, human; D051760:Xeroderma Pigmentosum Group A Protein; C086984:XPC protein, human; D002945:Cisplatin