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PubMed1987

Cytoprotective effects of disodium cromoglycate on rat stomach mucosa.

The cytoprotective effects of the anti-asthmatic drug, disodium cromoglycate (DSCG), on gastric mucosal necrosis induced by ethanol in rats were studied. Subcutaneous, but not oral, DSCG prevented the formation of gastric lesions and this effect was dose-dependent between 1.25 and 40 mg kg-1, with an ED50 value of 6.8 mg kg-1. Maximal cytoprotection occurred 15-30 min after DSCG treatment. Histological examination revealed that DSCG effectively protected the gastric mucosa against ethanol-induced vascular congestion, haemorrhage, epithelial desquamation and mucosal oedema. Enhanced production of endogenous prostaglandins, which are known cytoprotective compounds, could not explain the mucosal protection. At a dose of 40 mg kg-1, DSCG did not change prostaglandin E2 or 6-keto-prostaglandin F1 alpha concentrations in gastric mucosal tissue, although its cytoprotective activity was partially inhibited by prior treatment of the animals with indomethacin.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

The cytoprotective effects of bilirubin and biliverdin on rat hepatocytes and human erythrocytes and the impact of albumin.

The hypothesis that unconjugated bilirubin and biliverdin are cytoprotective antioxidants has been examined for the first time in systems containing cells. In primary rat hepatocytes exposed to xanthine oxidase and hypoxanthine, bilirubin (0-60 microM) failed to prolong cell survival. In contrast, biliverdin (20-100 microM) markedly delayed hepatocyte necrosis in a concentration-dependent manner. When 0.3 mM of albumin was present, bilirubin (0-50 microM) became protective of hepatocytes, while biliverdin was less dramatically enhanced in its cytoprotective effect. In human erythrocytes exposed to peroxyl radicals, bilirubin and biliverdin inhibited 50% cell lysis at lower concentrations than Trolox and ascorbate, respectively. Albumin alone appeared less cytoprotective in red cells than in hepatocytes, but its presence enhanced the effects of both pigments on erythrocytes. Of probable physiologic relevance, bilirubin with albumin present or biliverdin alone protected hepatocytes substantially (and to a lesser extent red cells) at the normal blood levels of bilirubin (3.4-26 microM). Moreover, the fact that the pigments are cytoprotective at higher bilirubin levels (e.g., 50-100 microM) tempts the speculation that they may be circulating cytoprotectors of overlooked importance in jaundice.

Animals↗
PubMed2004

Impaired cytoprotective function of muscle in human gallbladders with cholesterol stones.

Acute cholecystitis develops in gallbladders (GB) with excessive bile cholesterol (Ch). Increased membrane Ch content affects membrane function and may affect PGE(2) receptors involved in the cytoprotection against acute inflammation. This study was aimed at determining whether the cytoprotective response to PGE(2) is affected by lithogenic bile with Ch. Muscle cells from human GB with cholesterol stones (ChS) or pigment stones (PS) were obtained by enzymatic digestion. PGE(2) levels were measured by radioimmunoassay, and activities of superoxide dismutase (SOD) and catalase were assayed by spectrophotometry. The contraction in response to H(2)O(2) in muscle cells from PS was 14 +/- 0.3%, not different from normal controls, and decreased after the cells were incubated with Ch-rich liposomes (P < 0.05), which increase the Ch content in the plasma membranes. In muscle cells from GB with ChS, H(2)O(2)-induced contraction was only 9.2 +/- 1.3% and increased to 14 +/- 0.2% after Ch-free liposome treatment to remove Ch from the plasma membranes (P < 0.01). H(2)O(2) caused a similar increase in the levels of lipid peroxidation and PGE(2) content in muscle cells from GBs with ChS and PS. However, the activities of SOD and catalase were significantly lower in muscle cells from GBs with ChS compared with those with PS. The binding capacity of PGE(2) receptors was also significantly lower in muscle cells from GBs with ChS compared with those with PS. In conclusion, the cytoprotective response to reactive oxygen species is reduced in muscle cells from GBs with ChS despite a normal increase in the cellular levels of PGE(2). This impaired cytoprotective response may be due to a dysfunction of PGE(2) receptors with decreased binding capacity resulting from excessive Ch levels in the plasma membrane.

Catalase↗
PubMed1993

Adaptive cytoprotection in the small intestine: role of mucus.

Gastric mucosal injury induced by strong irritants can be dramatically reduced by pretreating the mucosa with mild forms of the same irritant. This phenomenon has been termed "adaptive cytoprotection." The aim of the present study was to use in vivo and in vitro approaches to study adaptive cytoprotection in the small intestine using physiologically relevant concentrations of oleic acid. Anesthetized rats were instrumented for perfusion of the proximal jejunum with 10 or 40 mM oleic acid (in 20 mM sodium taurocholate). Mucosal epithelial integrity was continuously monitored by measuring the blood-to-lumen clearance of 51Cr-labeled EDTA. Perfusion of the lumen with 40 mM oleic acid produced a 10-fold increase in 51Cr-EDTA clearance, which was not affected by a previous perfusion with 10 mM oleic acid, i.e., no adaptive cytoprotection. In another series of experiments, oleic acid was placed in the lumen rather than perfused, and mucosal epithelial integrity was assessed histologically. Intraluminal placement of 10 mM oleic acid resulted in the generation of a mucus layer over the epithelium. Subsequent placement of 40 mM oleic acid did not produce significant epithelial cell injury, i.e., adaptive cytoprotection. In in vitro studies, mucin (1, 5, and 10 mg/ml) was layered over confluent monolayers of Caco-2 cells prior to addition of 2 mM oleic acid in 4 mM sodium taurocholate. The epithelial cell injury induced by oleic acid was inhibited by mucin in a dose-dependent manner. Further studies indicate that mucin does not prevent, but simply delays, the onset of cell injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗
PubMed1993

Adaptive cytoprotection of the rat duodenum is not dependent on nitric oxide-induced changes in blood flow.

Mild irritation of the rat duodenum enhances mucosal resistance to acid via a prostaglandin-mediated mechanism. Prostaglandins increase mucosal blood flow, but it is not known whether such changes in blood flow significantly contribute to adaptive cytoprotection. We induced blood flow changes by manipulating the arginine-nitric oxide pathway, which is independent from prostaglandin synthesis, and determined the resulting effects on the cytoprotective response. In anesthetized rats, we tested the effects of intraduodenal infusion of mild acid on duodenal blood flow and on the prevention of mucosal damage by subsequent strong acid in control, indomethacin-pretreated, and NG-nitro-L-arginine-pretreated rats (NG-nitro-L-arginine inhibits the nitric oxide synthase). Additional experiments tested the effects of the prostaglandin analogue 16,16-dimethyl-prostaglandin (PG) E2 or sodium nitroprusside (nitric oxide donor) on duodenal blood flow and on mucosal protection against acid. Exposure of the duodenal mucosa to mild acid increased duodenal blood flow and mucosal resistance to acid. Instillation of 16,16-dimethyl-PGE2 also increased blood flow and mucosal resistance to acid. However, sodium nitroprusside increased blood flow without increasing mucosal resistance to acid, and NG-nitro-L-arginine inhibited the change in blood flow induced by acid while preserving the adaptive cytoprotection phenomenon intact. In conclusion, adaptive cytoprotection of the duodenal mucosa appears to be independent of changes in blood flow.

16,16-Dimethylprostaglandin E2↗
PubMed2001

Adenosine, oxidative stress and cytoprotection.

Adenosine, a metabolite of ATP, serves a number of important physiological roles in the body. These actions contribute to sedation, bradycardia, vasorelaxation, inhibition of lipolysis and regulation of the immune system and are mediated, in part, through activation of three distinct adenosine receptor (AR) subtypes. To date, four receptor types have been cloned: A1, A2A, A2B and A3. It is becoming increasing clear that adenosine contributes significantly to cytoprotection, a function mediated principally by the A1AR and A3AR. In this review, we survey the literature on the role of adenosine and the mechanisms underlying cytoprotection and ischemic preconditioning, a process characterized by cytoprotection derived from repeated brief ischemic challenges. An important recent observation is that the expression of several AR subtypes could be regulated by oxidative stress to provide a greater cytoprotective role. Thus, like other proteins known to be regulated during ischemia, the A1AR and A3AR can be considered as being inducible receptors.

Adenosine↗
PubMed1996

Phospholipase A2-induced cytoprotection of proximal tubules: potential determinants and specificity for ATP depletion-mediated injury.

Addition of phospholipase A2 (PLA2) to isolated proximal tubular segments (PTS) has previously been shown to decrease hypoxic cell death without altering ATP concentrations. The study presented here was undertaken to identify determinant(s) of this protection, and to define the spectrum of injuries against which it can operate. PTS were extracted from mouse kidneys and subjected to diverse forms of injury (hypoxia/reoxygenation, antimycin A, Ca2+ ionophore, amphotericin B, FeSO4, and myohemoglobin). In subtoxic doses, addition of PLA2 significantly reduced hypoxic- and antimycin A-induced injury (percentage of lactate dehydrogenase release); however, a dose-dependent exacerbation of all other forms of injury resulted. The ability of PLA2 to mitigate hypoxic injury remained intact despite the inhibition of Na,K-ATPase (ouabain) or the inducement of cytoskeletal disruption (cytochalasin D). However, it was negated by minimally toxic amphotericin B or Ca2+ ionophore doses, indicating its dependence on preserved ionic gradients. Nevertheless, neither lowering/removing buffer Ca2+ or NaCl concentrations, nor hypertonic mannitol addition reproduced the cytoprotective effect of PLA2. PLA2 induced synergistic deacylation in hypoxic tubules, suggesting that unsaturated fatty-acid accumulation might mediate its cytoprotective effect. The fact that the addition of exogenous arachidonate, but not palmitate, to tubules protected against hypoxia, but worsened nonhypoxic forms of injury, supported this hypothesis. Since arachidonate might induce "feedback" inhibition of intracellular PLA2, the ability of an intracellular phospholipase inhibitor (ONO-RS-082; Biomol, Plymouth, PA) to blunt hypoxic damage was tested. This agent fully reproduced the cytoprotective effect of PLA2. It was concluded that: (1) PLA2-induced cytoprotection is relatively specific for ATP depletion injury; (2) it is dependent on, but not explained by, maintenance of NaCl and Ca2+ gradients; (3) it does not require Na,K-ATPase activity or cytoskeletal integrity for its expression; and (4) extracellular PLA2, via arachidonate release, may cause feedback inhibition of intracellular PLA2, thereby protecting critical intracellular targets from attack.

Adenosine Triphosphate↗
PubMed1999

A risk-benefit assessment of amifostine in cytoprotection.

Recent advances in chemotherapy have focused on the benefit of high dose regimens, increasing the dose intensity of conventional chemotherapy and using intensified chemotherapy with or without autologous bone marrow rescue. Dose intensity usually increases objective response rates of antineoplastic drugs and might, in some circumstances, improves survival. However, unacceptable acute and/or cumulative toxicity often impairs the proper management of patients, leading to dose reduction or treatment delay, thus reducing the efficacy and potentially the quality of life of patients. Therefore, considerable efforts have been made to manage, to prevent, and to delay many acute and cumulative treatment-related toxicities. Amifostine (WR-2721 ) is a multiorgan cytoprotector which has demonstrated cytoprotective effects, in vitro and in vivo, against the most common cytotoxic drug-related toxicities and against radiation-induced adverse effects in healthy tissues. In vitro and in vivo, cytoprotection was observed in several organs including kidney, haematopoietic stem cells, myocardial cells, neural cells, and mucosa, without detectable protection of malignant cells. In addition, in preclinical studies, amifostine appeared to be able to reduce the risk of radiation-induced secondary neoplasms. Phase I studies showed that nausea/vomiting and hypotension are the dose-limiting toxicities of amifostine and these may be controlled by reducing the duration of injection of amifostine. Phase II and randomised studies have confirmed the efficacy of amifostine in protecting against radiotherapy-induced mucositis, cisplatin-induced nephrotoxicity, cyclophosphamide-induced neutropenia and carboplatin-induced thrombocytopenia. Importantly, the cytoprotection of healthy tissues occurred without any significant deleterious effect on response rate, time to progression, and survival of patients receiving amifostine. However, in addition to the potential quality of life benefit, the most important question of whether the use of a cytoprotective agent might translate into the possibility of maintaining the dose intensity of anticancer therapies has still to be answered. The real benefit of amifostine in the overall management of patients with cancer requires additional studies to determine whether this chemoprotective approach can be of benefit to patients by increasing response rate, time to progression, and long term survival in patients receiving the more recent combination therapies involving new drugs such as the taxanes and oxaliplatin.

Amifostine↗
PubMed1986

Cytoprotective effect of pirenzepine and palm wine on rats gastric mucosa.

Pirenzepine (Gastrozepin--Boechringer Ingelheim) is selective antimuscarinic blocker (MI-blocker) which has been used in the treatment of peptic ulcer because of its ability to reduce gastric acid secretion. But pirenzepine has also been found to have a cytoprotective effect on gastric mucosa in rats. The aim of the present investigation was to find out if palm wine also has any cytoprotective effect on rat gastric mucosa. Gastric mucosal ulcerations were induced with absolute ethanol. It was found that Pirenzepine induced 57% cytoprotection while palm wine induced 24% cytoprotection in rat gastric mucosa. The protection with the latter substance was not statistically significant, while the effect with pirenzepine was significant.

Animals↗
PubMed1996

Mucosal irritation, adaptive cytoprotection, and adaptation to topical ammonia in the rat stomach.

BACKGROUND: The urease-ammonia (NH4OH) system has been proposed to play a major role in the pathogenesis of the Helicobacter pylori-associated gastritis, but the mechanism of the mucosal damage has not been fully explained. This study was designed to examine possible adaptive cytoprotection and the adaptation of rat gastric mucosa to the irritant action of NH4OH and urease. METHODS AND RESULTS: Single application of NH4OH alone in various concentrations (15-500 mM) caused concentration-dependent mucosal damage starting with 30 mM and reaching a maximum at 250 mM NH4OH, similar to that obtained with 100% ethanol; it was accompanied by a decrease in gastric blood flow (GBF) to approximately 30% of the normal value. When the mucosa was first exposed to the low, non-damaging concentration (15 mM) of NH4OH and then insulted with 100% ethanol, the extent of ethanol damage was greatly attenuated as compared with that caused by ethanol alone. This adaptive cytoprotection was accompanied by the rise in GBF and reversed, in part, by the pretreatment with indomethacin, an inhibitor of prostaglandin (PG)-cyclooxygenase; with L-NAME, a blocker of NO-synthase; or with capsaicin deactivating the sensory nerves. Damaging concentrations of NH4OH (125 mM) caused widespread mucosal damage after the first application, but with repeated insults with 125 mM NH4OH a gradual reduction in the mucosal lesions, accompanied by enhanced mucosal cell proliferation and over-expression of epidermal growth factor (EGF) (using immunocytochemistry) and mRNA of EGF (using trans-reverse polymerase chain reaction), were observed. CONCLUSIONS: NH4OH alone damages gastric mucosa only at the concentration exceeding that found in H. pylori-infected stomachs, whereas at lower concentrations it acts as 'mild' irritant to induce adaptive cytoprotection. This adaptive cytoprotection appears to be mediated, in part, by endogenous PG, sensory nerves, and an arginine-NO-dependent pathway, and repeated applications of NH4OH induce gastric adaptation, probably mediated by enhanced expression of EGF and its receptors and by an increased cell proliferation.

Adaptation, Physiological↗
PubMed1998

[Cytoprotective effect of amifostine in children during induction therapy according to BFM-83: report on cases].

Amifostine is the agent of proved cytoprotective activity against alkylating drugs and rubidomycine. Its protective effect against other cytotoxic drugs is doubtful. BFM-83 induction therapy for ANLL (ARA-C + RUB + VP-16) which is applied to children with acute non-lymphoblastic leukemia (ANLL) commonly contributes to severe adverse reactions. We administered amifostine to three children: 2 boys with ANLL (7 and 11 yrs) and 1 girl with MDS (3 yrs) during etoposide and rubidomycine induction therapy in order to decrease chemotherapy-related adverse reactions. Doses of amifostine were 740 mg/m2, 910 mg/m2 and 910 mg/m2 respectively. Efficacy of the therapy was evaluated on the base of blast decline in the bone marrow, efficacy of the cytoprotection by myelo and nephrotoxicity symptoms analysis. Chemotherapy-related adverse effects in the children protected by amifostine were less severe and observed by the shorter periods as compared with the historical control group of 20 patients treated according to BFM-83 without cytoprotection. These cases show the potential beneficial effect of amifostine during BFM-83 induction therapy for ANLL. The further randomised clinical study of the proposed cytoprotection should be performed to establish its value.

Amifostine↗
PubMed2000

Cytoprotective effect of rabeprazole against ethanol-induced gastric mucosal damage: possible involvement of nitric oxide.

The cytoprotective effect of rabeprazole, a new proton pump inhibitor, against ethanol-induced gastric mucosal damage was investigated in rats. Rats received intraperitoneal injections of rabeprazole once only or once daily for 3 days. Subsequently, the rats were given 1 ml of absolute ethanol by oral intubation. Some rats given rabeprazole were treated with N-omega-nitro-L-arginine methyl ester (L-NAME) or indomethacin. Repeated administration of rabeprazole significantly inhibited ethanol-induced gastric mucosal damage, although single administration of this drug did not. Pretreatment with L-NAME abolished the cytoprotective effect of rabeprazole. This inhibitory effect of L-NAME was reversed by L-arginine but not by D-arginine. Pretreatment with indomethacin did not influence the cytoprotective effect of rabeprazole. These results suggest that repeated intraperitoneal administration of rabeprazole has a cytoprotective effect against ethanol-induced gastric mucosal damage and that this effect may be mediated via nitric oxide but not via prostaglandins.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMedDate not supplied

Clinical pharmacokinetics and metabolism of paclitaxel after polychemotherapy with the cytoprotective agent amifostine.

BACKGROUND: Cytoprotection of healthy cells represents a new approach in cancer chemotherapy, but a pharmacokinetic drug interaction between the cytostatic and the cytoprotectant is undesired. METHODS: The purpose was to evaluate the clinical pharmacokinetics (PHK) of paclitaxel (PACLI) and its metabolites under cytoprotection in patients suffering from breast cancer. PACLI was administered alone and in a second cycle in combination with amifostine (AMI) as a paired cross over. RESULTS: In both treatment schedules the steady state of PACLI occurred after 3 hours, the tmax of metabolites between 3 and 4 hours. The mean steady-state concentration was cmax = 5432 +/- 1238 ng/ml in the control group and cmax = 5140 +/- 2407 ng/ml in the AMI group. For the serum metabolites, the findings were very similar: 6-OH-PACLI: cmax 413 +/- 153 ng/ml versus 432 +/- 304 ng/ml, 3"-OH-PACLI: cmax 99 +/- 103 ng/ml versus 123 +/- 98 ng/ml, 3",6-DiOH-PACLI: cmax 43 +/- 55 ng/ml versus 75 +/- 85 ng/ml. AUC values of metabolites were slightly higher in the AMI group, but PHK seemed equal. CONCLUSION: The results gave evidence, that cytoprotection with AMI has no clinical consequences on PACLI pharmacokinetics and biotransformation.

Aged↗
PubMedDate not supplied

The cytoprotective effect of amifostine in acute radiation dermatitis: a retrospective analysis.

To study the impact of amifostine as a cytoprotective agent against acute radiation dermatitis, we reviewed 220 patient records. One hundred cancer patients, with tumors localised in the pelvis (bladder, rectum, prostatic carcinomas, or gynecological cancer), who received radiotherapy and cytoprotective treatment with intravenous infusion of amifostine (group A) were included in this study. Retrospectively, we randomly selected from a database in our hospital 120 historical controls, who received only radiotherapy without cytoprotection (group B). Mean gross dermatitis score (MGDS) was the mean value of recorded acute radiation dermatitis according to common toxicity criteria. In group A versus B patients, a significantly reduced severity of dermatitis (P < 0.001, Fisher's exact test) and significant reduction of MGDS as well as mean interruption treatment time (P < 0.001, Mann-Whitney U test) was observed. The relative risk of the outcome of the two study groups was 0.23 (95% CI: 0.15 to 0.34). The significant dermato-cytoprotective effect of amifostine noticed in our retrospective analysis warrants further investigation with randomised trials.

Adult↗
PubMed1992

Correlation between the cytoprotective effect of beta-carotene and its gastric mucosal level in indomethacin (IND) treated rats with or without acute surgical vagotomy.

As to earlier observations that beta-carotene prevents the development of gastric mucosal injury produced by different noxious agent, however, its cytoprotective effect can be abolished by acute surgical vagotomy. The aim of this study was to evaluate the possible correlation between the gastric mucosal cytoprotective effect of beta-carotene and its gastric mucosal level in rats treated with IND. The gastric mucosal damage was produced by the administration of IND (20 mg/kg s.c.). The instillation of beta-carotene and acute surgical vagotomy (ASV) or SHAM operation were carried out 30 min before IND treatment. The rats were sacrificed 4 h after IND application, and the number and severity of gastric mucosal erosions were noted. The blood rats was collected quantitatively, the liver and the gastric mucosa were removed, and the beta-carotene and vitamin A level of the gastric mucosa, serum and liver were measured with HPLC. It was found that: 1. Beta-carotene induced gastric cytoprotection in SHAM-operated rats treated with IND but its effect disappeared after ASV. 2. Although the beta-carotene level of the gastric mucosa increased its concentration was not elevated in the serum of intact and vagotomized animals either. 3. Vitamin A Formation was not detected in the liver of animals with or without ASV. It was concluded that the lack of intake of beta-carotene into the gastric mucosa can not play etiologic role in the failure of gastric cytoprotection of rats with acute bilateral surgical vagotomy.

Animals↗
PubMed1987

Gastric cytoprotection induced by prostaglandin-dopaminergic mechanism.

The cytoprotective effects on the gastric mucosa of the Bromocriptine, a peripheral dopaminergic receptor agonist compared with Misoprostol against ethanol-induced injury were studied. Pretreatment with SCH 23390 (a DA1 receptor antagonist) and Domperidone (a DA2 receptor antagonist), showed that Misoprostol was peripheral dopaminergic receptor dependent in the gastric cytoprotective mechanism, and that Bromocriptine was a selective peripheral DA2 receptor agonist in the gastric cytoprotection mechanism; as well as, indomethacin pretreatment, showed that peripheral DA2 receptors were endogenous prostaglandin dependent. In conclusion, a prostaglandin-dopaminergic mechanism was postulated in gastric cytoprotection.

Alprostadil↗
PubMedDate not supplied

Cytoprotective action of roxatidine acetate HCl.

The cytoprotective action of roxatidine acetate HCl (roxatidine) was investigated. We also studied the involvement of endogenous prostaglandins (PGs) in the cytoprotective action of roxatidine and the effect of roxatidine on SRS content in pleurisy induced by A23187. Simultaneously, these effects of roxatidine were compared with those of other histamine H2-receptor antagonists at the same anti-secretory activity level. Roxatidine prevented formation of the gastric mucosal lesions induced by abs. ethanol, 0.6 N HCl and 0.2 N NaOH, but it failed to prevent 30% NaCl-induced gastric mucosal lesions. Cimetidine, ranitidine and famotidine failed to prevent formation of the gastric mucosal lesions induced by necrotizing agents. The cytoprotective action of roxatidine was not abolished by pretreatment with indomethacin. Roxatidine did not greatly influence SRS production. Consequently, it appears that roxatidine has a cytoprotective action and that this action is not associated with endogenous PGs and SRS.

Animals↗
PubMed1986

[Cytoprotection of gastric mucosa induced by tripotassium-dicitrato bismuthate against ethanol stress. Dependent mechanisms of sulfhydryl, dopaminergic and endogenous prostaglandin].

In groups of white Wistar rats, the cytoprotective effect induced by TDB on the gastric mucosa against the ethanol injury, was studied; where macroscopic protection and histologic cytoprotection in gastric corpus was found, and no in antrum mucosa. The cytoprotective mechanism give by TDB, were studied by the test of Indomethacin, Cl2Hg, Domperidone, Chlorpromazine and Acetazolamide, where each drug was given as pretreatment. Was conclude that TDB give gastric cytoprotection by the mechanism of the nonprotein sulfhydryl, by to be one peripheral agonist of the neuronal dopamine receptors, by increase of endogenous prostaglandin, by little increment of cAMP and no participate the gastric bicarbonate secretion.

Acetazolamide↗