Tadalafil inhibits elevated glutamic oxaloacetic transaminase during alcohol aflatoxin induced hepatocellular carcinoma in rats

<p>Hepatocellular carcinoma is a type of primary liver cancer and dietary exposure to aflatoxins is one of major causative factor for the development of HCC. Present study was planned to assess the role of PDE5 inhibitor tadalafil on glutamic oxaloacetic transaminase during aflatoxin induced H...

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Main Authors: Divya Rawat (Author), Raj Kumar Koiri (Author)
Format: Book
Published: International Journal of Immunotherapy and Cancer Research - Peertechz Publications, 2020-02-25.
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LEADER 00000 am a22000003u 4500
001 peertech__10_17352_2455-8591_000022
042 |a dc 
100 1 0 |a Divya Rawat  |e author 
700 1 0 |a Raj Kumar Koiri  |e author 
245 0 0 |a Tadalafil inhibits elevated glutamic oxaloacetic transaminase during alcohol aflatoxin induced hepatocellular carcinoma in rats 
260 |b International Journal of Immunotherapy and Cancer Research - Peertechz Publications,   |c 2020-02-25. 
520 |a <p>Hepatocellular carcinoma is a type of primary liver cancer and dietary exposure to aflatoxins is one of major causative factor for the development of HCC. Present study was planned to assess the role of PDE5 inhibitor tadalafil on glutamic oxaloacetic transaminase during aflatoxin induced HCC. Rats of control group received normal food and water ad libitum. Alcohol and HCC group received chronic dose of alcohol via drinking water for two weeks. After two weeks HCC group received single dose of crude aflatoxin and allowed to develop HCC for six weeks. After six weeks, HCC rats were post-treated with tadalafil via drinking water for 10 days. Result revealed that PDE5 inhibitor tadalafil treatment reduced glutamic oxaloacetic transaminase level and SGOT activity in liver towards normal in HCC rats suggesting its therapeutic potential.</p> 
540 |a Copyright © Divya Rawat et al. 
546 |a en 
655 7 |a Research Article  |2 local 
856 4 1 |u https://doi.org/10.17352/2455-8591.000022  |z Connect to this object online.