Experimental hyperprolinemia induces mild oxidative stress, metabolic changes, and tissue adaptation in rat liver


Autoria(s): Ferreira, Andrea G. K.; da Cunha, Aline A.; Machado, Fernanda R.; Pederzolli, Carolina D.; Dalazen, Giovana R.; de Assis, Adriano M.; Lamers, Marcelo L.; Santos, Marinilce Fagundes dos; Dutra-Filho, Carlos S.; Wyse, Angela T. S.
Contribuinte(s)

UNIVERSIDADE DE SÃO PAULO

Data(s)

24/10/2013

24/10/2013

2012

Resumo

The present study investigated the effects of chronic hyperprolinemia on oxidative and metabolic status in liver and serum of rats. Wistar rats received daily subcutaneous injections of proline from their 6th to 28th day of life. Twelve hours after the last injection the rats were sacrificed and liver and serum were collected. Results showed that hyperprolinemia induced a significant reduction in total antioxidant potential and thiobarbituric acid-reactive substances. The activities of the antioxidant enzymes catalase and superoxide dismutase were significantly increased after chronic proline administration, while glutathione (GSH) peroxidase activity, dichlorofluorescin oxidation, GSH, sulfhydryl, and carbonyl content remained unaltered. Histological analyses of the liver revealed that proline treatment induced changes of the hepatic microarchitecture and increased the number of inflammatory cells and the glycogen content. Biochemical determination also demonstrated an increase in glycogen concentration, as well as a higher synthesis of glycogen in liver of hyperprolinemic rats. Regarding to hepatic metabolism, it was observed an increase on glucose oxidation and a decrease on lipid synthesis from glucose. However, hepatic lipid content and serum glucose levels were not changed. Proline administration did not alter the aminotransferases activities and serum markers of hepatic injury. Our findings suggest that hyperprolinemia alters the liver homeostasis possibly by induction of a mild degree of oxidative stress and metabolic changes. The hepatic alterations caused by proline probably do not implicate in substantial hepatic tissue damage, but rather demonstrate a process of adaptation of this tissue to oxidative stress. However, the biological significance of these findings requires additional investigation. J. Cell. Biochem. 113: 174183, 2012. (C) 2011 Wiley Periodicals, Inc.

Conselho Nacional de Desenvolvimento Cientifico e Tecnologico

Conselho Nacional de Desenvolvimento Cientifico e Tecnologico

Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq-Brazil)

Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq), Brazil

Fundacao de Amparo a Pesquisa do Estado do Rio Grande do Sul (FAPERGS)

Fundacao de Amparo a Pesquisa do Estado do Rio Grande do Sul (FAPERGS)

Identificador

JOURNAL OF CELLULAR BIOCHEMISTRY, MALDEN, v. 113, n. 1, supl. 1, Part 1, pp. 174-183, JAN, 2012

0730-2312

http://www.producao.usp.br/handle/BDPI/35906

10.1002/jcb.23342

http://dx.doi.org/10.1002/jcb.23342

Idioma(s)

eng

Publicador

WILEY-BLACKWELL

MALDEN

Relação

JOURNAL OF CELLULAR BIOCHEMISTRY

Direitos

closedAccess

Copyright WILEY-BLACKWELL

Palavras-Chave #HYPERPROLINEMIA #HISTOLOGICAL ANALYSIS #OXIDATIVE STRESS #LIVER #SERUM #GLYCOGEN CONTENT #ANTIOXIDANT POTENTIAL TRAP #CEREBRAL-CORTEX #ANIMAL-TISSUES #BLOOD LACTATE #AMINO-ACIDS #IN-VIVO #PROLINE #CELLS #BRAIN #APOPTOSIS #BIOCHEMISTRY & MOLECULAR BIOLOGY #CELL BIOLOGY
Tipo

article

original article

publishedVersion