NDLI: Estudio Del Mecanismo De Fosforilación De Proteínas Como Respuesta Celular Hepática Inducida Por Adriamicina, Con O Sin Protección Con L-carnitina

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Estudio Del Mecanismo De Fosforilación De Proteínas Como Respuesta Celular Hepática Inducida Por Adriamicina, Con O Sin Protección Con L-carnitina

Content Provider	Semantic Scholar
Author	Celular, Sección De Biología
Copyright Year	2006
Abstract	The changes in the pattern of protein phosphorylation have been associated to numerous pathologies of different origins and severity; these alterations can be linked to oxidative stress and subsequent modifications in the protein kinases and phosphatases. In this regard, adriamycin therapy have been related to the heart and liver oxidative stress and organ disfunction. Therefore, in addition to the heart, the liver might be another adriamycin toxic target. However, adriamycin liver alterations have been poorly studied. The aim of this work was to determined liver protein phosphorylation before and after adriamycin administration. Female Sprague-Dawley rats (n=3), 40-60g body weight, were randomized into four groups: control, adriamycin, carnitine and adriamycin-carnitine. Saline adriamycin (15mg/Kg body weight) and carnitine (20 mg before adriamycin) were given intravenously (0,1 ml). Samples from the medium liver lobe were taken for biochemical experiments including phosphorylation with (a 32 -P) ATP, inmunodetection of phosphoproteins in serine and tirosine, JNK and C-jun proteins. The protein phosphorylation was different between the groups studied. The greater expression of protein phosphorylates was determined in the adriamycin group. We suggest that there is a relationship between carnitine administration and decreased expression of protein phosphorylates. Carnitine may be a hepatoprotector. Key words: Adriamicine, liver, protein phosphorylation, L-carnitine, JNK, C-jun.
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://files.bvs.br/upload/S/0001-5504/2006/v57n1/a01.pdf
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

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