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At least 1,207 records · Page 67Linked to original sources
PubMedDate not supplied

Cytoprotective effects of hematopoietic growth factors on primary human acute myeloid leukemias are not mediated through changes in BCL-2, bax, or p21WAF1/CIP1.

BACKGROUND: Hematopoietic growth factors (HGF) can suppress chemotherapy-induced programmed cell death (apoptosis) in hematopoietic cells. Although HGF can modulate the expression of apoptosis-regulatory genes, including bcl-2, bax, and p21WAF1/CIP1 in cell lines, few data address whether HGF regulate the expression of these proteins in primary acute myeloid leukemia (AML). MATERIALS AND METHODS: We evaluated the expression of bcl-2, bax, and p21WAF1/CIP1 in primary samples from patients with AML in the presence and absence of HGF. The potential association of HGF-induced changes in the levels of these proteins with inhibition of chemotherapy-induced apoptosis was further investigated. RESULTS: While a combination of steel factor (SF) and PIXY321 inhibited etoposide-induced apoptosis in 8/11 primary AML samples studied, Bcl-2 and bax protein levels were unaffected by exposure to HGF and/or etoposide. In contrast, HGF enhanced basal and etoposide-induced p21WAF1/CIP1 protein levels in 9/11 and 7/11 of the cases, respectively. In several cases, inhibition of apoptosis by HGF was seen without up-regulation of p21WAF1/CIP1 levels, suggesting that modulation of p21WAF1/CIP1 is not required for HGF-mediated inhibition of apoptosis. CONCLUSIONS: These data indicate that HGF-mediated inhibition of chemotherapy-induced apoptosis in primary AML samples is not mediated through changes in Bcl-2, bax, and p21WAF1/CIP1 protein levels.

Adult↗
PubMed1998

Administration of the cytoprotectant amifostine.

This article provides guidelines for the use of amifostine (Ethyol, Alza Pharmaceuticals, Palo Alto, CA, and U.S. Bioscience, Inc., West Conshohocken, PA), a pancytoprotective agent approved for reducing renal toxicity associated with cisplatin administration in patients with advanced ovarian or non-small cell lung cancer. Pretreatment with amifostine reduces the incidence of serious and cumulative chemotherapy-induced toxicities, thus improving quality of life, and allows administration of optimal doses and scheduling of chemotherapy and radiation therapy, translating into improved survival. Practical guidelines for administration of amifostine are provided in an effort to ameliorate emesis, amifostine's principle side effect.

Amifostine↗
PubMed1999

Experimental cirrhosis of the liver and cytoprotective effects of alpha tocopherol.

OBJECTIVE: To investigate whether alpha tocopherol (alpha-T) treatment influences liver cirrhosis induced by carbon tetrachloride (CCl4) in the rat. DESIGN: Laboratory experiment. SETTING: Teaching hospital, Turkey. SUBJECTS: Fifty rats were divided into three groups. Group I consisted of ten controls; Group II: twenty CCl4 induced cirrhotic rats and Group III: twenty cirrhotic rats treated with Vitamin E. INTERVENTIONS: Experimental cirrhosis was induced in rats by subcutaneous administration of 0.4 ml CCl4 (diluted 1:4 with olive oil) per kilogram body weight twice a week for 12 weeks. MAIN OUTCOME MEASURES: Histopathologically evaluation of liver, liver malondialdehyde and glutathione peroxidase levels and aspartate aminotransferase (SGOT), alanine aminotransferase (SGPT) and gamma-glutamyltranspeptidase (GGT) levels. RESULTS: Histopathologic evaluation of liver samples demonstrated cirrhotic changes in CCl4 treated groups. The enzyme levels in Group II were significantly increased (p < 0.05) but it was insignificantly lower in the alpha tocopherol treated group III. In Group II, statistically significant increase in liver malondialdehyde levels was determined (p < 0.001). CONCLUSION: Our results demonstrate that alpha-T administration may protect liver against CCl4 induced cirrhosis.

Analysis of Variance↗
PubMed1999

[Vitamin C: structure-activity correlation and cytoprotective actions through free radical scavenging and extracellular matrix construction].

Conventional studies on vitamin C have been conducted by single-dosage administration with ascorbic acid itself being so labile as to undergo irreversible degradation. In contrast, enrichment of intracellular ascorbate is accomplished by pro-vitamin C in which its 2,3-enediol moiety is protected with phosphate ester, being thereafter enzymatically esterolyzed. Ascorbic acid-2-O-phosphate (Asc2P) gradually releases ascorbate, which is cumulatively taken up into diverse human or mammalian cells, and prevents cell injuries such as post-ischemic reperfusional injury in the liver or heart, age-dependent telomeric DNA shortening in endothelial or epithelial cells, UV-B irradiational injury in the skin and lipid peroxide-induced injury in the vascular endothelium, and tumor invasion and metastasis.

Animals↗
PubMed2000

Ferriporphyrins and endothelium: a 2-edged sword-promotion of oxidation and induction of cytoprotectants.

Heme arginate infusions blunt the symptoms of patients with acute intermittent porphyria without evidence of the vascular or thrombotic side effects reported for hematin. To provide a rationale for heme arginate's safety, the present study examined the effects of various ferriporphyrins to sensitize human endothelial cells to free radical injury and to induce heme oxygenase and ferritin expression. Heme arginate, unlike hematin, did not amplify oxidant-induced cytotoxicity mediated by hydrogen peroxide (5.3 +/- 2.4 versus 62.3 +/- 5.3% (51)Cr release, P <.0001) or by activated neutrophils (14.4 +/- 2.9 versus 41.1 +/- 6.0%, P <.0001). Nevertheless, heme arginate efficiently entered endothelial cells similarly to hematin, since both markedly induced heme oxygenase mRNA (more than 20-fold increase) and enzyme activity. Even with efficient permeation, endothelial cell ferritin content was only minimally increased by heme arginate compared with a 10-fold induction by hematin; presumably less free iron was derived from heme arginate despite up-regulation of heme oxygenase. Hematin is potentially vasculopathic by its marked catalysis of oxidation of low-density lipoprotein (LDL) to endothelial-toxic moieties. Heme arginate was significantly less catalytic. Heme arginate-conditioned LDL was less than half as cytotoxic to endothelial cells as hematin-conditioned LDL (P <.004). It is concluded that heme arginate may be less vasculotoxic than hematin since it is an effective heme oxygenase gene regulator but a less efficient free-radical catalyst.

Arginine↗
PubMedDate not supplied

Study of interaction of gastroenterological agents in the presence of cytoprotective drugs. Part I: Adsorption of the chosen inhibitors of histamine H2 receptors on sucralfat in vitro.

We investigated adsorption of the chosen histamine H2 receptor inhibitors on sucralfat. Evaluation of adsorption was conducted by statistic methods in vitro taking into account environment reaction and sucralfat form. The obtained results prove that the tested therapeutic substances are adsorbed on sucralfat in all used pH ranges and the ability of sucralfat bounding depends on its form and environment reaction. The highest adsorption value was observed in the samples with pH 3.6 in the presence of sucralfat suspension, and the lowest in environment pH 1.5 in the presence of sucralfat paste. From among the tested histamine receptors ranitidine hydrochloride is adsorbed in the best way and cimetidine hydrochloride and famotidine in much worse way.

Adsorption↗
PubMedDate not supplied

Cytotoxicity, cytoprotection and neurotoxicity of novel deprenyl-related propargylamines, stable nitroxide free radicals, in vitro and in vivo.

Since novel synthesized deprenyl-related derivatives of nitroxides, named "JSAKs", have been shown to possess antioxidative properties, their cytotoxicity on neuronal-like PC-12 cells line was examined. The antiproliferative effect of two selected JSAKs was examined and expressed as IC10, IC50 and IC90, and compared with those of the parent nitroxide (Nx-640), model nitroxide TEMPO and deprenyl. There were substantial differences in the dose-dependence of all the observed antiproliferative and cytotoxic effects. Compared to anticancer drugs and apoptosis inducers with topoisomerase inhibitor properties (etoposide and camptothecin), novel compounds displayed cytotoxicity at considerably higher concentrations. The dose-dependent anti-apoptotic potency of JSAKs and Nx-640 was also investigated and compared to TEMPO and deprenyl effects. The observed structure-dependent correlation was very encouraging and prompted us to screen and to compare the in vivo time-dependent effects of JSAKs, Nx-640 and deprenyl administration on the rat intact nigrostriatal neurocytes. TH-immunochemistry was applied as the test method and marker for the changes in the state of the rat catecholaminergic system, also giving evidence that low-toxic and cell-permeable JSAKs can cross the blood-brain barrier, which is the mandatory prerequisite for the therapeutic application of antioxidants and drugs to the brain. Taken together, it can be concluded with great certainty that novel deprenyl-related JSAKs might be especially good candidates for further anticancer investigations in vitro and in vivo and future pharmacological applications.

Animals↗
PubMed2004

[Potentialities of cytoprotection in the treatment of chronic heart failure in patients with coronary heart disease].

The study was undertaken to evaluate the effects of long-term (6-month) therapy with the selective beta-blocker bisoprolol, the cytoprotector trimetazidine and their combination on the clinical course of disease, the morphofunctional parameters of the left ventricle (LV) and life quality in 71 patients with coronary heart disease (CHD) concurrent with functional classes (FC) III-IV chronic heart failure (CHF) (ejection fraction (EF) < 35%, as evidenced by echoCG). In Groups 1, 2, and 3, basic therapy was supplemented by bisoprolol, trimetazidine, and bisoprolol plus trimetazidine, respectively. The initial dose of bisoprolol was 1.25 mg with its subsequent titration to an individually tolerable. Trimetazidine was given in a dose of 20 mg thrice daily. The patients' clinical status and echoCG were monthly assessed. There was a decrease in FC of CHD in all the groups, a reduction in LV end diastolic and systolic volumes, and an increase in shortening faction, LV EF, and an improvement of LV diastolic function. There was evidence that it should be expedient and safe to use the cytoprotector trimetazidine in the treatment of CHF in patients with CHD. In patients with CHD concurrent with CHF, therapy using a combination of bisoprolol and trimerazidine was found to have the most pronounced impact, which yielded the maximum clinical and hemodynamic effect (LV EF increased by 42.6% of the baseline values, the rate of early and late ventricular diastolic filling decreased by 59% of the baseline values). The revealed regularities of the positive effect on the clinical and hemodynamic parameters of long-use of bisoprolol, trimetazidine, and their combination in patients with CHD concurrent with FC III-IV CHF show it expedient to include these drugs and their combination into therapy for CHF that develops in the presence of CHD.

Aged↗