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Chemical Compound Review:

AC1MHYOP (2S)-2-amino-4-[[(1S)-1-[3,4- bis[(1S)-1...

Synonyms: CCRIS 8801, LS-72522, 119212-33-8, 2,3,5-(Trigsyl)HQ, 2,3,5-(Triglutathion-S-yl)hydroquinone

Hill, B.A. et al., Hill, B.A. et al., Lau, S.S. et al.

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Disease relevance of 2,3,5-(Trigsyl)HQ

To address the issue of the differential potency of these conjugates we investigated the metabolism and toxicity of 2,3,5-(triGSyl)HQ and 2-(GSyl)HQ in the in situ perfused rat kidney [1].

High impact information on 2,3,5-(Trigsyl)HQ

The gamma-GT-mediated hydrolysis of 2,3,5-(triGSyl)HQ was lowest in the hamster, and this species were not susceptible to the renal toxicity of this conjugate [2].
Infusion of 5 and 10 mumol 2,3,5-(triGSyl)HQ into the right renal artery caused a time-dependent elevation in gamma-glutamyl transpeptidase (gamma-GT) excretion into urine produced by both the perfused and the contralateral kidneys [1].
To determine whether mitochondria are targets for 2,3,5-(triGSyl)HQ, the in vivo and in vitro effects of this conjugate on rat renal mitochondria (RRM) were investigated [3].
The effects of 2,3,5-(triGSyl)HQ on state 4 respiration preceded significant elevations in blood urea nitrogen, which occurred at 8 hr [3].

Anatomical context of 2,3,5-(Trigsyl)HQ

Although the cellular target(s) for 2,3,5-(triGSyl)HQ is not known, substantial evidence implicates mitochondria as the primary cellular target for aliphatic S-conjugates [3].

Analytical, diagnostic and therapeutic context of 2,3,5-(Trigsyl)HQ

Using HPLC-EC to analyze urine and bile, metabolites of 2,3,5-(triGSyl)HQ (10 mumol) were observed only within the first 30 min of perfusion [1].

References

Metabolism of 2-(glutathion-S-yl)hydroquinone and 2,3,5- (triglutathion-S-yl)hydroquinone in the in situ perfused rat kidney: relationship to nephrotoxicity. Hill, B.A., Davison, K.L., Dulik, D.M., Monks, T.J., Lau, S.S. Toxicol. Appl. Pharmacol. (1994) [Pubmed]
Metabolism as a determinant of species susceptibility to 2,3,5-(triglutathion-S-yl)hydroquinone-mediated nephrotoxicity. The role of N-acetylation and N-deacetylation. Lau, S.S., Kleiner, H.E., Monks, T.J. Drug Metab. Dispos. (1995) [Pubmed]
The effects of 2,3,5-(triglutathion-S-yl)hydroquinone on renal mitochondrial respiratory function in vivo and in vitro: possible role in cytotoxicity. Hill, B.A., Monks, T.J., Lau, S.S. Toxicol. Appl. Pharmacol. (1992) [Pubmed]

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