LIVER RESPONSE TO THE CONSUMPTION OF FRIED SUNFLOWER OIL.

fried sunflower oil growing rats lipid toxicity liver oxidative stress

Journal

The Journal of nutritional biochemistry
ISSN: 1873-4847
Titre abrégé: J Nutr Biochem
Pays: United States
ID NLM: 9010081

Informations de publication

Date de publication:
06 Aug 2024
Historique:
received: 28 05 2024
revised: 16 07 2024
accepted: 05 08 2024
medline: 9 8 2024
pubmed: 9 8 2024
entrez: 8 8 2024
Statut: aheadofprint

Résumé

Sunflower oil is one of the most commonly used fat sources in Argentina, and deep-fat frying is the popular food preparation process. The liver response of feeding a diet containing fried sunflower oil (SFOx) on growing rats was studied. Thirty-nine male weanling Wistar rats were randomly assigned to one of three diets for 8 wks: control (C), a sunflower oil (SFO) and a diet containing SFOx, both of the sunflower diets were mixed with a commercial rat chow at weight ratio of 13% (w/w). Body weight and food consumption were recorded weekly. At t=8 wk, lipid profile and glycemia were measured. Visceral adiposity was registered. Liver was weighed and preserved for histological analysis, relative fatty acid profile, fibrosis markers and oxidative status. The three diets did not alter body weights; however, the SFOx fed rats showed increased energy intake and visceral fat; therefore, in liver saturated fat content, trans fatty acids, plus other unidentified minor components, such as hydroperoxides, hydroxides, epidioxides, hydroperoxy epidioxides, hydroxylepidioxides, and epoxides, were detected. The hepatosomatic index of SFOx rats was altered and showed hepatic steatosis. SFOx rats exhibited increased liver dichlorodihydrofluorescein-diacetate and thiobarbituric acid substance levels and oxidized-proteins content. Their livers had lower relative levels of monounsaturated, polyunsaturated fatty acids and catalase activity, but matrix metalloproteinase-9 activity was unchanged. Consumption of a diet rich in fried oil during growth could induce liver damage due to steatosis, excessive lipid toxicity and the accumulation of reactive oxygen species. Further progression could lead to hepatic fibrosis.

Identifiants

pubmed: 39117077
pii: S0955-2863(24)00165-7
doi: 10.1016/j.jnutbio.2024.109734
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

109734

Informations de copyright

Copyright © 2024. Published by Elsevier Inc.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Elisa V Macri (EV)

Universidad de Buenos Aires, Facultad de Odontología, Cátedra de Bioquímica General y Bucal. Buenos Aires, Argentina.

Vanessa Touceda (V)

Universidad de Buenos Aires, Facultad de Odontología, Cátedra de Bioquímica General y Bucal. Buenos Aires, Argentina; Pontificia Universidad Católica Argentina. Facultad de Medicina. Instituto de Investigaciones Biomédicas (UCA-CONICET). Laboratorio de Patología Cardiovascular Experimental e Hipertensión Arterial. Buenos Aires, Argentina.

Morena Wiszniewski (M)

Universidad de Buenos Aires, Facultad de Odontología, Cátedra de Bioquímica General y Bucal. Buenos Aires, Argentina; Universidad de Buenos Aires. Facultad de Medicina, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Centro de Estudios Farmacológicos y Botánicos (CEFYBO), Laboratorio de Endocrinología Molecular (LEM). Buenos Aires, Argentina.

Leonardo D Cacciagiu (LD)

Universidad de Buenos Aires, Facultad de Odontología, Cátedra de Bioquímica General y Bucal. Buenos Aires, Argentina; Hospital General de Agudos Teodoro Álvarez. Laboratorio Central. Sección Bioquímica. Buenos Aires, Argentina.

Valeria Zago (V)

Universidad de Buenos Aires, Facultad de Farmacia y Bioquímica. Instituto de Fisiopatología y Bioquímica Clínica (INFIBIOC). Laboratorio de Lípidos y Aterosclerosis, Hospital de Clínicas. INFIBIOC-UBA, Buenos Aires, Argentina.

Susana Puntarulo (S)

Universidad de Buenos Aires, Facultad de Farmacia y Bioquímica, Fisicoquímica, Argentina. National Council for Science and Technology (CONICET)- Universidad de Buenos Aires, Instituto de Bioquímica y Medicina Molecular (IBIMOL), Buenos Aires, Argentina.

Néstor Pellegrino (N)

Department of Bromatology, School of Pharmacy and Biochemistry, University of Buenos Aires Argentina, Junin 956- 2nd Floor, 1113 Buenos Aires, Argentina.

Fima Lifshitz (F)

Professor of Pediatrics Emeritus. State University of New York, Downstate Medical Center, College of Medicine, Brooklyn. Santa Barbara, Honorary Professor, University of Buenos Aires, Argentina CA, USA.

Silvia M Friedman (SM)

Universidad de Buenos Aires, Facultad de Odontología, Cátedra de Bioquímica General y Bucal. Buenos Aires, Argentina.

Verónica Miksztowicz (V)

Universidad de Buenos Aires, Facultad de Odontología, Cátedra de Bioquímica General y Bucal. Buenos Aires, Argentina; Pontificia Universidad Católica Argentina. Facultad de Medicina. Instituto de Investigaciones Biomédicas (UCA-CONICET). Laboratorio de Patología Cardiovascular Experimental e Hipertensión Arterial. Buenos Aires, Argentina. Electronic address: veronica.miksztowicz@odontologia.uba.ar.

Classifications MeSH