Batcioglu, KadirYildirim, BattalSatilmis, BasriUyumlu, Ayse BurcinGenc, Metin FikretBentli, RecepDjamgoz, Mustafa B. A.2024-08-042024-08-0420160250-46851303-829Xhttps://doi.org/10.1515/tjb-2016-0040https://search.trdizin.gov.tr/yayin/detay/224911https://hdl.handle.net/11616/92461Objective: Nitric oxide synthase and arginase are frequently antagonistic and interactive, although both use L-arginine as common substrate. Their balance is of potential functional importance. How the balance changes in cancer is unknown. Increasing evidence suggests that progression of carcinomas involves functional voltage-gated sodium channel (VGSC) activity. Methods: The present study extended this study to liver and aimed to determine whether (i) DMBA carcinogenesis would affect the activities of arginase and NOS and (ii) treatment with Na-channel blocker RS100642 would ameliorate the impact of the carcinogen on the arginase-NOS balance. Results: DMBA application significantly increased arginase activity and, correspondingly, the level of L-ornithine by 25-33%. In contrast, NOS activity decreased by 11%. Importantly, RS100642 treatment completely suppressed the effect on arginase. Conclusion: It is concluded (i) that DMBA carcinogenesis changes the hepatic arginase-NOS balance, increasing the overall dominance of arginase and (ii) that VGSC inhibition has a protective effect on liver.eninfo:eu-repo/semantics/openAccessLiverCarcinogenesisArginaseNitric oxide synthaseSodium channelsRS100642Article41427527910.1515/tjb-2016-00402-s2.0-84982787930Q4224911WOS:000387205500007Q4