Tags

Type your tag names separated by a space and hit enter

Acetaminophen-induced toxicity is prevented by beta-D-glucan treatment in mice.
Eur J Pharmacol. 2006 Aug 14; 543(1-3):133-40.EJ

Abstract

The protective effect of beta-glucan against oxidative injury caused by acetaminophen was studied in mice liver. BALB-c mice (25-30 g) were pre-treated with beta-d-glucan (50 mg/kg, p.o.) for 10 days and on the 11th day they received an overdose of acetaminophen (900 mg/kg, i.p.). Four hours after the acetaminophen injection, mice were decapitated and their blood was taken to determine serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH) and tumor necrosis factor-alpha (TNF-alpha) levels. Tissue samples of the liver were taken for histological examination or for the determination of levels of malondialdehyde, an end product of lipid peroxidation; glutathione (GSH), a key antioxidant; and myeloperoxidase activity, an index of tissue neutrophil infiltration. The formation of reactive oxygen species in hepatic tissue samples was monitored by using the chemiluminescence technique with luminol and lucigenin probes. Acetaminophen caused a significant decrease in the GSH level of the tissue, which was accompanied with significant increases in the hepatic luminol and lucigenin chemiluminescence values, malondialdehyde level, MPO activity and collagen content. Similarly, serum ALT, AST levels, as well as LDH and TNF-alpha, were elevated in the acetaminophen-treated group when compared with the control group. On the other hand, beta-d-glucan treatment reversed all these biochemical indices, as well as histopathological alterations that were induced by acetaminophen. In conclusion, these results suggest that beta-d-glucan exerts cytoprotective effects against oxidative injury through its antioxidant properties and may be of therapeutic use in preventing acetaminophen toxicity.

Authors+Show Affiliations

Marmara University, School of Pharmacy, Department of Pharmacology, Istanbul, Turkey.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

16822497

Citation

Toklu, Hale Z., et al. "Acetaminophen-induced Toxicity Is Prevented By beta-D-glucan Treatment in Mice." European Journal of Pharmacology, vol. 543, no. 1-3, 2006, pp. 133-40.
Toklu HZ, Sehirli AO, Velioğlu-Oğünç A, et al. Acetaminophen-induced toxicity is prevented by beta-D-glucan treatment in mice. Eur J Pharmacol. 2006;543(1-3):133-40.
Toklu, H. Z., Sehirli, A. O., Velioğlu-Oğünç, A., Cetinel, S., & Sener, G. (2006). Acetaminophen-induced toxicity is prevented by beta-D-glucan treatment in mice. European Journal of Pharmacology, 543(1-3), 133-40.
Toklu HZ, et al. Acetaminophen-induced Toxicity Is Prevented By beta-D-glucan Treatment in Mice. Eur J Pharmacol. 2006 Aug 14;543(1-3):133-40. PubMed PMID: 16822497.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Acetaminophen-induced toxicity is prevented by beta-D-glucan treatment in mice. AU - Toklu,Hale Z, AU - Sehirli,A Ozer, AU - Velioğlu-Oğünç,Ayliz, AU - Cetinel,Sule, AU - Sener,Göksel, Y1 - 2006/06/02/ PY - 2005/12/02/received PY - 2006/05/17/revised PY - 2006/05/18/accepted PY - 2006/7/11/pubmed PY - 2006/12/12/medline PY - 2006/7/11/entrez SP - 133 EP - 40 JF - European journal of pharmacology JO - Eur J Pharmacol VL - 543 IS - 1-3 N2 - The protective effect of beta-glucan against oxidative injury caused by acetaminophen was studied in mice liver. BALB-c mice (25-30 g) were pre-treated with beta-d-glucan (50 mg/kg, p.o.) for 10 days and on the 11th day they received an overdose of acetaminophen (900 mg/kg, i.p.). Four hours after the acetaminophen injection, mice were decapitated and their blood was taken to determine serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH) and tumor necrosis factor-alpha (TNF-alpha) levels. Tissue samples of the liver were taken for histological examination or for the determination of levels of malondialdehyde, an end product of lipid peroxidation; glutathione (GSH), a key antioxidant; and myeloperoxidase activity, an index of tissue neutrophil infiltration. The formation of reactive oxygen species in hepatic tissue samples was monitored by using the chemiluminescence technique with luminol and lucigenin probes. Acetaminophen caused a significant decrease in the GSH level of the tissue, which was accompanied with significant increases in the hepatic luminol and lucigenin chemiluminescence values, malondialdehyde level, MPO activity and collagen content. Similarly, serum ALT, AST levels, as well as LDH and TNF-alpha, were elevated in the acetaminophen-treated group when compared with the control group. On the other hand, beta-d-glucan treatment reversed all these biochemical indices, as well as histopathological alterations that were induced by acetaminophen. In conclusion, these results suggest that beta-d-glucan exerts cytoprotective effects against oxidative injury through its antioxidant properties and may be of therapeutic use in preventing acetaminophen toxicity. SN - 0014-2999 UR - https://www.unboundmedicine.com/medline/citation/16822497/Acetaminophen_induced_toxicity_is_prevented_by_beta_D_glucan_treatment_in_mice_ DB - PRIME DP - Unbound Medicine ER -