Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Malondialdehyde (MDA) derivatives occur as normal constituents of rat and human urine. In a previous study, it was found that MDA excretion in rats is responsive to MDA intake and to certain factors that increase lipid peroxidation in vivo: vitamin E deficiency, iron administration and a high concentration of cod liver oil (CLO) fatty acids in the tissues. In the present study, the effect on MDA excretion of several additional dietary and endogenous factors was evaluated. The composition of dietary fatty acids had a major influence on MDA excretion in fed animals, being highest for animals fed n-3 fatty acids (20:5 and 22:6) from CLO, intermediate for those fed n-6 (18:2) acids from corn oil (CO) and lowest for those fed saturated acids from hydrogenated coconut oil (HCO). Diet was the main source of urinary MDA in all groups. Fasting produced a marked increase in urinary MDA, which tended to be higher in rats previously fed CLO. Fasting MDA excretion was not affected by the level of CO in the diet (5, 10 or 15%), indicating that feeding n-6 acids does not increase lipid peroxidation in vivo. Adrenocorticotropic hormone and epinephrine administration increased urinary MDA, further indicating that lipolysis either releases fatty acid peroxides from the tissues or increases the susceptibility of mobilized fatty acids to peroxidation. A decrease in fasting MDA excretion was observed in rats previously fed a high level of antioxidants (vitamin E + BHT + vitamin C) vs a normal level of vitamin E. MDA excretion increased following adriamycin and CCl4 administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Response of urinary malondialdehyde to factors that stimulate lipid peroxidation in vivo. 282 43

Fluorescence emission from the single tryptophan residues of two melanocyte stimulating hormones, alpha-MSH and delta-MSH, and their quenching kinetics were studied in aqueous solution and in reverse micelles of AOT/water/isooctane. Incorporation into micelles caused blue shifted and narrower emission peaks, altered quantum yields and considerably enhanced anisotropies for both peptides when compared to emission from bulk water. The variation of emission parameters with micellar water content was interpreted to suggest that while the tryptophan in alpha-MSH lies in close vicinity of the water-AOT molecular interface, that in delta-MSH is solubilized in the central water pool. Total emission intensity decays followed complex (biexponential) kinetics in both aqueous and micellar media. Although the mean lifetimes for both peptides were always nearly the same, the average rotational correlation times in micelles for alpha-MSH were three times as much as those for delta-MSH. Stern-Volmer plots obtained using acrylamide and CCl4 as quenchers localized in the micellar and organic pseudophases, respectively, were non-linear and dependent on emission wavelength. Quenching by acrylamide was more efficient for delta-MSH than for alpha-MSH, while the opposite was true for quenching by CCl4. The implication of this result for localization of the peptides in micelles was consistent with the earlier one emerging from these studies.
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PMID:Fluorescence study of melanocyte stimulating hormones in AOT reverse micelles. 768 63

Transforming growth factor beta1 (TGF-beta1) is a pleiotropic cytokine, which displays potent profibrogenic effects and is highly expressed in fibrotic livers. For this reason, development of TGF-B1 inhibitors might be of great importance to control liver fibrogenesis as well as other undesired side effects due to this cytokine. Potential peptide inhibitors of TGF-beta1 (derived from TGF-beta1 and from its type III receptor) were tested in vitro and in vivo using different assays. Peptides P11 and P12, derived from TGF-beta1, and P54 and P144, derived from its type III receptor, prevented TGF-beta1-dependent inhibition of MV1Lu proliferation in vitro and markedly reduced binding of TGF-beta1 to its receptors. P144 blocked TGF-beta1-dependent stimulation of a reporter gene under the control of human alpha2(I) collagen promoter. Intraperitoneal administration of P144 also showed potent antifibrogenic activity in vivo in the liver of rats receiving CCl4. These rats also showed a significant decrease in the number of activated hepatic stellate cells as compared with those treated with saline only. These results suggest that short synthetic peptides derived from TGF-beta1 type III receptor may be of value in reducing liver fibrosis in chronic liver injury.
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PMID:A synthetic peptide from transforming growth factor beta type III receptor inhibits liver fibrogenesis in rats with carbon tetrachloride liver injury. 1294 1