Drugs online research references
ciit.org
To better understand the molecular mechanisms of the pleiotropic responses induced by exposure to peroxisome proliferator chemicals (PPCs), we conducted a systematic search for genes whose mRNA levels are modulated by the PPC WY-14,643 (WY) in rat liver. The sequence of one up-regulated cDNA (2480 bp) was predicted to encode a protein of 735 aa with 82% identity to the porcine 17 beta-hydroxysteroid dehydrogenase type IV (HSD IV). Like the porcine enzyme, the rat HSD IV contains' a region homologous to yeast hydratase-dehydrogenase-epimerases and to sterol carrier proteins, indicating that the rat HSD IV has broad substrate specificity and contributes to cholesterol metabolism. The rat HSD IV was regulated by diverse PPCs via two distinct mechanisms. Induction of HSD IV and acyl-CoA oxidase (ACO) proteins in rat liver at different treatment times and concentrations of gemfibrozil and di-n-butyl phthalate were almost identical, indicating that HSD IV mRNA induction involves the peroxisome proliferator-activated receptor alpha, a regulator of ACO. In contrast, HSD IV protein levels were only weakly induced by WY, a strong inducer of ACO protein, even though the levels of HSD IV and ACO mRNA were strongly stimulated by WY and gemfibrozil. Thus, HSD IV protein levels were uniquely regulated pretranslationally by WY via a novel mechanism. Increased conversion of estradiol to the less-active estrone by HSD IV induction may explain how phthalate exposure leads to decreases in serum estradiol levels and suppression of ovulation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8913347&dopt=Abstract
Life Sci. 1991;48(11):1091-9.
Influence of fibric acid derivatives on intermediate filament proteins in myocardiocyte cultures.
Gonzalez FJ, Aranega AE, Linares A, Fernandez JE, Muros MA, Velez C, Alvarez L, Aranega A.
Departament of Morphological Sciences, School of Medicine, University of Granada, Spain.
We analyzed desmin and vimentin accumulation in chick myocardiocyte cultures treated with the fibric acid derivatives bezafibrate, fenofibrate and gemfibrozil. The most noteworthy finding was the 50% decrease in the cytoplasmic desmin fraction in cells treated with gemfibrozil in comparison to control cultures, and the 19% increase in the cytoskeletal fraction in cultures treated with gemfibrozil and with bezafibrate. Vimentin accumulation by cells treated with bezafibrate was similar to that in control cultures, however the cytoskeletal vimentin fraction rose by 26% after treatment with gemfibrozil, and fell 13% after treatment with fenofibrate. No vimentin was found in the cytoplasmic fraction of cell treated with bezafibrate. Given the role of intermediate filaments in heart muscle contraction, fibric acid derivative- induced changes in the cytoplasmic and cytoskeletal concentrations of intermediate filament proteins may be related with the secondary effects of these drugs on heart rate.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1997786&dopt=Abstract
Int J Cardiol. 1991 Oct;33(1):47-54.
Effects of fibric acid derivatives on accumulation of actin in myocardiocytes.
Aranega A, Gonzalez FJ, Aranega AE, Muros MA, Fernandez JE, Velez C, Prados J, Alvarez L.
Basic Cardiovascular Research Section, School of Medicine, University of Granada, Spain.
We used sodium dodecylsulphate polyacrylamide gel electrophoresis and immunoblotting to analyze the effects of the fibric acid derivatives bezafibrate, fenofibrate and gemfibrozil on the accumulation of actin in the cytoplasmic and cytoskeletal fraction of cultured myocardiocytes. All three drugs tested modified cellular and subcellular actin in different ways, and the findings are thought to be related with the secondary effect of arrhythmia known to be caused by these drugs. Bezafibrate and gemfibrozil more markedly affected accumulation of actin by myocytes, while fenofibrate interfered less notably with the accumulation of this protein.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1937982&dopt=Abstract
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