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Cefadroxil potency as cancer co-therapy candidate by glutathione s-transferase mechanism

Author(s): Tri Yuliani | Sudibyo Martono | Sansan Sukamdani Tjipto | Muhammad Yusuf Putroutomo | Irwan Desyanto Raharjo Indartono

Journal: International e-Journal of Science, Medicine & Education
ISSN 2231-8194

Volume: 7;
Issue: 1;
Start page: 15;
Date: 2013;
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Keywords: GSTs | cefadroxil | specific substrates | in vivo | co-therapy

Background: Glutathione S-transferases (GSTs) havean important role in the detoxification of electrophiles,such as some anticancer drugs. Compounds with phenolicand/or α,b-unsaturated carbonyl group have been knownas GSTs inhibitor in vitro. Cefadroxil in vitro decreasedGST-Pi activity but not GSTs in rat kidney cytosol.GST inhibitor in a specific organ and of a specific classis needed for safety in cancer chemotherapy. The studyaims to observe the effect of cefadroxil on GSTs in vivoin rat kidney cytosol and then compare it to those seenfor liver, lung, and spleen in vivo.Methods: Cefadroxil was given twice a day byforcefeeding for five days. Rat kidney cytosol was thenprepared and its protein concentration was determined.Cytosolic total GST, GST-Mu and GST-Pi activitieswere monitored by a continuous spectrophotometricmethod using the following substrates: 1-chloro,2,4-dinitrobenzene (CDNB) (non-specific substrate),1,2-dichloro-4-nitrobenzene (DCNB) for GST-Mu, andethacrynic acid (EA) for GST-Pi.Results: The data showed that cefadroxil significantlyincreased the activity of GSTs, GST-Mu, and GSTPiin rat kidney cytosol (8.75%, 47.81%, and 6.67%respectively).Conclusion: Cefadroxil did not inhibit GSTs, GST-Mu,and GST-Pi in rat kidney in vivo indicating that it doesnot inhibit chemotherapy detoxification by GSTs, GSTMu,and GST-Pi in normal kidney cells.

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