Change in liver and plasma ceramides during D-galactosamine-induced acute hepatic injury by LC-MS/MS

Bioorganic & Medicinal Chemistry Letters
Miho YamaguchiShosuke Kojo

Abstract

In fulminant hepatic failure, various toxins causing multi-organ failure increase in plasma. As a novel toxin, ceramide, a well-studied lipid mediator of apoptosis, levels were determined by LC-MS/MS in the liver and plasma of D-galactosamine-intoxicated rats. 18 and 24h after intraperitoneal administration of D-galactosamine (1g/kg body weight) to rats, fulminant hepatic failure occurred as evidenced by a severe elevation in plasma GOT and GPT. The liver concentration of minor ceramide components (C18:0, C20:0, C22:1, C22:0, and C24:2) increased significantly compared to that in the control group that was given saline. The plasma concentration of major ceramides (C24:0, C24:1, C16:0, C22:0, C22:1, and C18:0) increased 24h after administration of D-galactosamine and the total ceramide concentration was also increased to 3.6 times that in the control. In conclusion, the increased concentrations of ceramides in plasma during fulminant hepatic failure may be one of important toxins causing damage in other organs including the brain and kidney.

References

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Citations

Dec 13, 2006·Lipids·Ikuyo IchiUNKNOWN Kisei Cohort Study Grooup
Apr 23, 2010·Biological & Pharmaceutical Bulletin·Yukiko WashinoShosuke Kojo
May 9, 2007·Journal of Nutritional Science and Vitaminology·Ikuyo IchiShosuke Kojo
Jan 1, 2008·Phytomedicine : International Journal of Phytotherapy and Phytopharmacology·Anshu RathiShanta Mehrotra
Mar 31, 2015·Expert Opinion on Therapeutic Targets·Lara BelliniHervé Le Stunff
Mar 15, 2006·Bioorganic & Medicinal Chemistry Letters·Hitomi NishiokaShosuke Kojo
May 22, 2021·Journal of the American College of Cardiology·Nadia AkawiCharalambos Antoniades
Jan 27, 2005·Journal of Mass Spectrometry : JMS

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis