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Ribose cysteine protects against acetaminophen-induced hepatic and renal toxicity
A M Lucas1, G Hennig, P K Dominick
1Department of Pharmaceutical Sciences, University of Connecticut, Storrs 06269-2092, USA.
Toxicologic Pathology
|October 12, 2000
Summary
Ribose cysteine (RibCys) protects against acetaminophen (APAP)-induced kidney damage. This cysteine prodrug reduced APAP toxicity and covalent binding in both liver and kidney tissues.
Area of Science:
- Toxicology
- Pharmacology
- Biochemistry
Background:
- Acetaminophen (APAP) overdose causes severe liver and kidney damage.
- Ribose cysteine (RibCys) is a cysteine prodrug known to protect against APAP-induced liver toxicity by increasing glutathione levels.
- The potential of RibCys to protect against APAP-induced kidney injury remains to be fully elucidated.
Purpose of the Study:
- To investigate the efficacy of RibCys in preventing acetaminophen-induced kidney damage in a murine model.
- To assess the impact of RibCys on APAP covalent binding to proteins in both hepatic and renal tissues.
Main Methods:
- Mice were administered APAP alone or in combination with RibCys.
- Liver and kidney toxicity were evaluated using plasma sorbitol dehydrogenase (SDH) and blood urea nitrogen (BUN) levels, respectively.
- Histopathological examination and assessment of APAP covalent binding to proteins were performed.
Main Results:
- APAP treatment led to significant elevations in SDH and BUN, indicating severe liver and kidney damage.
- Co-administration of RibCys with APAP normalized SDH and BUN levels, comparable to control groups.
- Histopathology confirmed the absence of hepatic and renal necrosis in RibCys-treated mice.
- RibCys cotreatment significantly decreased APAP covalent binding to hepatic and renal proteins.
Conclusions:
- Ribose cysteine effectively protects against both acetaminophen-induced liver and kidney toxicity.
- RibCys mitigates APAP-induced nephrotoxicity by reducing covalent binding of APAP metabolites to cellular proteins.
- This cysteine prodrug demonstrates significant therapeutic potential for preventing APAP-induced organ damage.
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