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Proceedings Paper

In vivo N-acetyl cysteine reduce hepatocyte death by induced acetaminophen
Author(s): Chih-Ju Lin; Feng-Chieh Li; Sheng-Shun Wang; Hsuan-Shu Lee; Chen-Yuan Dong
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Paper Abstract

Acetaminophen (APAP) is the famous drug in global, and taking overdose Acetaminophen will intake hepatic cell injure. Desptie substantial progress in our understanding of the mechanism of hepatocellular injury during the last 40 years, many aspects of the pathophysiology are still unknown or controversial.1 In this study, mice are injected APAP overdose to damage hepatocyte. APAP deplete glutathione and ATP of cell, N-Acetyl Cysteine (NAC) plays an important role to protect hepatocytes be injury. N-Acetyl Cysteine provides mitochondrial to produce glutathione to release drug effect hepatocyte. By 6-carboxyfluorescein diacetate (6-CFDA) metabolism in vivo, glutathione keep depleting to observe the hepatocyte morphology in time. Without NAC, cell necrosis increase to plasma membrane damage to release 6-CFDA, that's rupture. After 6-CFDA injection, fluorescence will be retained in hepatocyte. For cell retain with NAC and without NAC are almost the same. With NAC, the number of cell rupture decreases about 75%.

Paper Details

Date Published: 2 June 2011
PDF: 8 pages
Proc. SPIE 8092, Medical Laser Applications and Laser-Tissue Interactions V, 80921L (2 June 2011); doi: 10.1117/12.889621
Show Author Affiliations
Chih-Ju Lin, National Taiwan Univ. (Taiwan)
Feng-Chieh Li, National Taiwan Univ. (Taiwan)
Sheng-Shun Wang, National Taiwan Univ. (Taiwan)
Hsuan-Shu Lee, National Taiwan Univ. Hospital (Taiwan)
Chen-Yuan Dong, National Taiwan Univ. (Taiwan)


Published in SPIE Proceedings Vol. 8092:
Medical Laser Applications and Laser-Tissue Interactions V
Ronald Sroka; Lothar D. Lilge, Editor(s)

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