PMID- 23507776
OWN - NLM
STAT- MEDLINE
DCOM- 20130903
LR  - 20211021
IS  - 1420-3049 (Electronic)
IS  - 1420-3049 (Linking)
VI  - 18
IP  - 3
DP  - 2013 Mar 18
TI  - The ameliorative effects of L-2-oxothiazolidine-4-carboxylate on 
      acetaminophen-induced hepatotoxicity in mice.
PG  - 3467-78
LID - 10.3390/molecules18033467 [doi]
AB  - The aim of the study was to investigate the ameliorative effects and the 
      mechanism of action of L-2-oxothiazolidine-4-carboxylate (OTC) on acetaminophen 
      (APAP)-induced hepatotoxicity in mice. Mice were randomly divided into six 
      groups: normal control group, APAP only treated group, APAP + 25 mg/kg OTC, APAP 
      + 50 mg/kg OTC, APAP + 100 mg/kg OTC, and APAP + 100 mg/kg N-acetylcysteine (NAC) 
      as a reference control group. OTC treatment significantly reduced serum alanine 
      aminotransferase and aspartate aminotransferase levels in a dose dependent 
      manner. OTC treatment was markedly increased glutathione (GSH) production and 
      glutathione peroxidase (GSH-px) activity in a dose dependent manner. The contents 
      of malondialdehyde and 4-hydroxynonenal in liver tissues were significantly 
      decreased by administration of OTC and the inhibitory effect of OTC was similar 
      to that of NAC. Moreover, OTC treatment on APAP-induced hepatotoxicity 
      significantly reduced the formation of nitrotyrosin and terminal deoxynucleotidyl 
      transferase dUTP nick end labeling positive areas of liver tissues in a dose 
      dependent manner. Furthermore, the activity of caspase-3 in liver tissues was 
      reduced by administration of OTC in a dose dependent manner. The ameliorative 
      effects of OTC on APAP-induced liver damage in mice was similar to that of NAC. 
      These results suggest that OTC has ameliorative effects on APAP-induced 
      hepatotoxicity in mice through anti-oxidative stress and anti-apoptotic 
      processes.
FAU - Choi, Jiwon
AU  - Choi J
AD  - Department of Radiological Sciences, Jeonju University, Jeonju 560-759, Korea. 
      jwchoi@jj.ac.kr
FAU - Park, Kwang-Hyun
AU  - Park KH
FAU - Kim, Sung Zoo
AU  - Kim SZ
FAU - Shin, Jun Ho
AU  - Shin JH
FAU - Jang, Seon-Il
AU  - Jang SI
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130318
PL  - Switzerland
TA  - Molecules
JT  - Molecules (Basel, Switzerland)
JID - 100964009
RN  - 0 (Aldehydes)
RN  - 0 (Analgesics, Non-Narcotic)
RN  - 0 (Antioxidants)
RN  - 0 (Thiazolidines)
RN  - 3604-79-3 (3-nitrotyrosine)
RN  - 362O9ITL9D (Acetaminophen)
RN  - 42HK56048U (Tyrosine)
RN  - 4Y8F71G49Q (Malondialdehyde)
RN  - EC 1.11.1.9 (Glutathione Peroxidase)
RN  - EC 2.6.1.1 (Aspartate Aminotransferases)
RN  - EC 2.6.1.2 (Alanine Transaminase)
RN  - EC 3.4.22.- (Casp3 protein, mouse)
RN  - EC 3.4.22.- (Caspase 3)
RN  - GAN16C9B8O (Glutathione)
RN  - K1CVM13F96 (4-hydroxy-2-nonenal)
RN  - SZB83O1W42 (Pyrrolidonecarboxylic Acid)
RN  - X7063P804E (2-oxothiazolidine-4-carboxylic acid)
SB  - IM
MH  - Acetaminophen/*toxicity
MH  - Alanine Transaminase/blood
MH  - Aldehydes/metabolism
MH  - Analgesics, Non-Narcotic/*toxicity
MH  - Animals
MH  - Antioxidants/*pharmacology/therapeutic use
MH  - Apoptosis/drug effects
MH  - Aspartate Aminotransferases/blood
MH  - Caspase 3/metabolism
MH  - Chemical and Drug Induced Liver Injury/blood/*prevention & control
MH  - DNA Fragmentation
MH  - Glutathione/metabolism
MH  - Glutathione Peroxidase/metabolism
MH  - Liver/drug effects/metabolism
MH  - Male
MH  - Malondialdehyde/metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Necrosis/chemically induced/prevention & control
MH  - Oxidative Stress/drug effects
MH  - Pyrrolidonecarboxylic Acid/*pharmacology/therapeutic use
MH  - Thiazolidines/*pharmacology/therapeutic use
MH  - Tyrosine/analogs & derivatives/metabolism
PMC - PMC6270228
EDAT- 2013/03/20 06:00
MHDA- 2013/09/04 06:00
PMCR- 2013/03/18
CRDT- 2013/03/20 06:00
PHST- 2013/01/23 00:00 [received]
PHST- 2013/01/31 00:00 [revised]
PHST- 2013/03/14 00:00 [accepted]
PHST- 2013/03/20 06:00 [entrez]
PHST- 2013/03/20 06:00 [pubmed]
PHST- 2013/09/04 06:00 [medline]
PHST- 2013/03/18 00:00 [pmc-release]
AID - molecules18033467 [pii]
AID - molecules-18-03467 [pii]
AID - 10.3390/molecules18033467 [doi]
PST - epublish
SO  - Molecules. 2013 Mar 18;18(3):3467-78. doi: 10.3390/molecules18033467.