15
Views
6
CrossRef citations to date
0
Altmetric
Original Article

Inhibition of Radiation-induced Changes of Glyoxalase I Activity in Mouse Spleen and Liver by Phenothiazines

&
Pages 403-410 | Received 10 Jan 1994, Accepted 06 Dec 1994, Published online: 03 Jul 2009
 

Abstract

Swiss albino mice (male) were irradiated with γ-rays at a dose-rate of 0·05 Gy s−1, and the activities of glyoxalase I (GI) and glyoxalase II (GII) were determined after 24 h in the spleen and liver. Radiation up to 4 Gy increased the activity of GI and decreased that of GII. It was possible that the radiation-induced changes in the activity of the glyoxalase system, particularly that of GI, were suggestive of the regeneration status of the tissue. Phenothiazines such as chlorpromazine (CPZ), promethazine (PMZ) and trimeprazine (TMZ) inhibited the radiation-enhanced activity of GI in a concentration-dependent manner. On the other hand, almost no change in the activity of GII was observed using phenothiazines. The effect of phenothiazines on radiation-induced changes of glyoxalase activity were reversed in the presence of ferrous (Fe2+) ions. However, phenothiazines inhibited the radiation effect in the presence of ferric (Fe3+) ions. This combined effect was predominant in the liver. A possible mechanism for the modifying effect of phenothiazines is suggested.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.