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1.
Eur. j. anat ; 22(4): 335-343, jul. 2018. ilus, graf
Artigo em Inglês | IBECS | ID: ibc-179097

RESUMO

Methyl parathion is one of the highly toxic organophosphorus (OP) compounds. It induces hepatotoxicity, which might be related to generation of reactive oxygen species. This study was carried out to investigate the protective roles of vitamins C and ginger against hepatotoxicity induced by methyl parathion in male albino rats.Sixty male albino rats were randomly divided into 6 groups (ten rats each). Group I was considered as controls. Animals of groups II, III and IV were given methyl parathion (2 mg/kg), ginger (200 mg/kg) and vitamin C (100 mg/kg) respectively. Groups V and VI were given ginger (200 mg/kg) and vitamin C (100 mg/kg) respectively 2 hours before methyl parathion administration. All animals were treated orally, once daily, for four weeks. Blood and liver samples were obtained for biochemical, immunohistochemistry and histopathological examinations.Administration of either ginger or vitamin C along with methyl parathion significantly reduced the alanine aminotransferase (ALT) and malondialdehyde (MDA) levels in rats compared to those only treated with methyl parathion. Treatment with either ginger or vitamin C in combination with methyl parathion resulted in increased level of reduced glutathione compared to the methyl parathion treated group. However, oral ginger significantly increased glutathione-S-transferase levels compared to the control group, and this may outbalance the protective value of ginger over vitamin C to guard against liver injury and oxidative stress. The immunohistochemical and histopathological examinations showed that ginger or vitamin C combination with methyl parathion resulted in less hepatocytes degeneration and milder portal tract infiltration compared to the methyl parathion group.In conclusion, pre-treatment with either ginger or vitamin C appears to alleviate methyl parathion-inducted hepatotoxicity. However, their protective role is still limited and needs further investigation


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Assuntos
Animais , Ratos , Metil Paration/toxicidade , Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle , Estresse Oxidativo/imunologia , Ácido Ascórbico/uso terapêutico , Gengibre , Fígado/anatomia & histologia , Glicogênio Hepático/análise , Metil Paration/administração & dosagem , Inseticidas/toxicidade , Ácido Ascórbico/administração & dosagem , Substâncias Protetoras/uso terapêutico , Fígado/ultraestrutura
2.
Rev. esp. enferm. dig ; 108(10): 672-676, oct. 2016. tab, ilus
Artigo em Inglês | IBECS | ID: ibc-156755

RESUMO

Glycogenic hepatopathy is a rare and underecognized complication in long-standing poorly controlled type 1 diabetes mellitus patients. This is a distinct entity from other causes of hepatomegaly and elevated liver enzymes in diabetics, such as nonalcoholic fatty liver disease. Glycogenic hepatopathy is characterized by the combination of poorly controlled diabetes, acute liver injury with marked elevation in serum aminotransferases, and the characteristic histological features on liver biopsy. It is important to distinguish this entity as it has the potential for resolution following improved glycemic control. In this report, we describe four cases of adult patients presenting elevated serum transaminases and hepatomegaly with a history of poorly controlled type I diabetes mellitus. One of the patients had also elevated amylase and lipase in the serum, without clinical or imagiologic evidence of acute pancreatitis. Liver biopsy was performed in all patients and revealed glycogenic hepatopathy. Clinician’s awareness of glycogenic hepatopathy should prevent diagnostic delay or misdiagnosis and will provide better insight and management for this condition (AU)


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Assuntos
Humanos , Glicogênio Hepático/análise , Hepatite/etiologia , Diabetes Mellitus Tipo 1/complicações , Transaminases/sangue , Amilases/sangue , Lipase/sangue
3.
An. vet. Murcia ; 17: 11-18, ene. 2001. tab, ilus
Artigo em Es | IBECS | ID: ibc-23374

RESUMO

Se estudia la cantidad y distribución del glucógeno hepático en 30 animales de raza bovina, de 4 años de edad, lidiados en plazas de toros permanentes de la Región de Murcia. Los niveles de glucógeno en los hígados de los animales lidiados son menores que en los controles y la distribución en el lobulillo hepático es centrolobulillar a diferencia de los animales control, que es panlobulillar, lo que indica que en las zonas perilobulillares es donde primero comienza la formación de glucosa a partir del glucógeno y su liberación a la circulación sanguínea. Además se observa una menor cantidad de glucógeno hepático en los animales con mayor debilidad durante la lidia (AU)


Assuntos
Animais , Bovinos , Histocitoquímica/normas , Glicogênio Hepático , Doenças dos Bovinos/diagnóstico , Propionatos , Hematoxilina/análise , Hepatopatias/veterinária , Glicogênio/análise , Glicogênio
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