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PubMedDate not supplied

A survey of the effects of loop diuretics on the zonulae occludentes of the perilymph-endolymph barrier by freeze fracture.

The acute (30 min) effects of the loop diuretics piretanide, ethacrynic acid, bumetanide, furosemide, and azosemide, and the chronic (8 days) effects of furosemide and bumetanide on the zonulae occludentes (tight junctions) of the perilymph-endolymph barrier in the stria vascularis and in Reissner's membrane of the basal cochlear turns were studied by freeze-fracture. Quantitative analysis of their effects indicated that the structural integrity of the barrier was modified by either as increase or a decrease in the number, depth, and density of the strands of the tight junctions of the strial marginal cells. Only azosemide appeared to modify the tight junctions between the epithelial cells of Reissner's membrane, but it had little effect on the strial junctions. The tight junctions between the basal cells of the stria appeared to be the least affected by the various loop diuretics, although piretanide appeared to increase randomly the intercellular spaces lying between the strands.

Animals↗
PubMed1991

Glutathione and glutathione conjugate efflux from cultured liver cells.

Efflux of glutathione (GSH) and GSH-conjugates from cultured rat liver epithelial cell lines; the non-tumorigenic ARL-15C1 and the gamma-glutamyl transpeptidase containing, tumorigenic ARL-16T2, has been assessed under basal condition and during chronic treatment with 75 and 150 microM ethacrynic acid (EA). The intracellular level of GSH increased in proportion to EA concentration during chronic exposure. The rates of GSH and GSH-EA conjugate efflux increased with intracellular GSH in both ARL cell lines. Glutathione-S-transferase activity measured with EA as substrate increased over the experimental time course after treatment with 150, but not 75 microM EA. When intracellular GSH content was increased by treatment with the cysteine pro-drug, 2-L-oxothiazolidine 4-carboxylic acid, the rate of GSH efflux was increased, but not the rate of GS-EA conjugate export. Inhibition of gamma-glutamyl transpeptidase by acivicin (AT-125) increased the GSH and GS-EA conjugate efflux rate in ARL-16T2 cells by factors of approximately 2 and 15, respectively. Acivicin treatment of ARL-16T2 cells chronically treated with EA elevated GSH efflux rate by 10-fold and GS-EA efflux by 40-fold versus control samples. These studies show that GSH and GSH conjugate efflux are accomplished as independently regulated processes. Efflux of GSH is enhanced by increased intracellular GSH, but increase in the conjugate transport rate requires the presence of the GSH conjugate. The response of the efflux process to treatment with a chronic GSH depleting agent was identical in two cell lines in which the metabolic fate of glutathione is known to differ fundamentally.

Animals↗
PubMed1995

Mechanisms of cell volume regulation in the proximal segment of the Malpighian tubule of Rhodnius neglectus.

The cell volume regulation of the lower segment cells of the Malpighian tubule of Rhodnius neglectus in anisosmotic media was evaluated by using video-optic techniques. When the medium osmolality was increased with addition of 100 mM mannitol the cells shrank to a minimum of 16.84 +/- 2.62% and subsequently swelled towards their initial volume undergoing a typical regulatory volume increase (RVI). Replacement of either K+ or Cl- or HCO(3-) by Na+, gluconate and phosphate, respectively, abolished the RVI response. Furthermore, the substitution of Na+ by tetramethylammonium (TMA+) in isosmotic conditions led to cellular swelling and death. Addition of either amiloride 10(-4) M, anthracene-9-COOH 5 x 10(-4) M, furosemide 5 x 10(-4) M or ethacrynic acid 5 x 10(-5) M, also abolished RVI. On the other hand, addition of either Ba2+ 10(-3) M, SITS 5 x 10(-4) M, ouabain 10(-3) M or vanadate 10(-3) M, did not change the RVI response. When the tubules were incubated in hyperosmotic media with EGTA 2 mM or verapamil 10(-6) M, the RVI response was abolished. In contrast, a decrease of NaCl concentration from 129 to 79 mM induced a cell swelling to a maximum of 33.11 +/- 1.73%, but the cells maintained swollen, only partially regulating their volume. These results show that the proximal cells of Malpighian tubule of R. neglectus are able to regulate their volume in hyperosmotic but only partially regulating in hyposmotic solutions. The mechanisms in RVI involve Na+, K+, Cl-, Ca2+ and HCO(3-) transport pathways and a ouabain-insensitive ATPase stimulated by Na+.

Animals↗
PubMedDate not supplied

Potentiation of ototoxicity by glutathione depletion.

The combination of 10 mg/kg ethacrynic acid (ETA) and 100 mg/kg kanamycin (KA) caused neither morphologic damage to the cochlea nor change in the auditory brain stem response of the chinchilla. However, after pretreatment with a single dose of buthionine sulfoximine (BSO; 800 mg/kg intraperitoneally) to reduce intracellular glutathione (gamma-glutamylcysteinylglycine; GSH) levels, the above single administration of ETA and KA resulted in complete deafness and severe morphologic damage. The kidney, which has a rapid GSH turnover and is therefore especially susceptible to GSH depletion by BSO, also demonstrated severe damage after this treatment. A similar rapid turnover of GSH and resulting limited capacity to detoxify reactive metabolites and free radicals may determine cochlear and renal vulnerability to this toxicity. These findings may explain the clinical observations of enhanced ototoxicity in patients administered amino-glycoside antibiotics concomitantly with loop diuretics.

Animals↗
PubMed1979

Coupling of NaHCO3 and NaCl reabsorption in dog kidneys during changes in plasma PCO2.

To study the relationship between proximal tubular reabsorption of bicarbonate, sodium, and chloride, the effects of changes in plasma PCO2 were examined in anesthetized dogs. Distal tubular reabsorption was inhibited by ethacrynic acid; plasma bicarbonate concentration was kept constant at 33.4 +/- 0.3 mM; glomerular filtration rate (GFR) was varied over a wide range to examine glomerulotubular balance (constant fractional reabsorption). Hypercapnia (PCO2, 112.0 +/- 2.5 mmHg) increased bicarbonate reabsorption by about 30%, and hypocapnia (PCO2, 19.8 +/- 0.6 mmHg) decreased reabsorption of bicarbonate by more than 50% and altered reabsorption of sodium, chloride, and bicarbonate in the molar ratios 2.7:1.6:1, respectively. During hypercapnia the range of glomerulotubular balance was extended to a GFR 125% of control. During hypocapnia glomerulotubular balance was present only at GFR below 50% of control; reabsorption of bicarbonate sodium, and chloride was constant at GFR exceeding 50% of control. During metabolic acidosis hypercapnia had no significant effect on reabsorption of bicarbonate, sodium, and chloride. These observations support the hypothesis that bicarbonate reabsorption is the main driving force for osmotic reabsorption of water and NaCl in the proximal tubules.

Acidosis↗
PubMedDate not supplied

Induction of rat liver glutathione transferase isoenzyme 7-7 by lead nitrate.

The glutathione transferase (GST) activity of rat liver cytosolic preparations with ethacrynic acid (EA) and (+/-)-7 beta, 8 alpha-dihydroxy-9 alpha, 10 alpha-epoxy-7,8,9,10-tetrahydro-benzo(a)pyrene (BPDE) as substrates, increased by 125 and 350%, respectively, in animals that had been treated with a single intravenous dose of Pb(NO3)2 (100 mumol/kg body wt) 48 h prior to sacrifice, whereas activity with 1-chloro-2,4-dinitrobenzene (CDNB) increased only about 60%. No induction of these activities was observed in cytosolic preparations from regenerating rat liver, whereas cytosols prepared from hepatocyte nodules showed increased activity with all three substrates (EA: 400%; BPDE: 790%; CDNB: 205%). These results suggest that Pb(NO3)2 is an inducer of GST 7-7, an isoenzyme that has been associated with hepatocarcinogenesis. Elucidation of the mechanism of GST 7-7 induction by lead may contribute to our understanding of the process of chemical carcinogenesis.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed1981

A search for a defect of proximal transport in denervated kidneys of conscious dogs.

The influence of renal nerves on proximal Na+ reabsorption was studied in clearance experiments with unilaterally renal-denervated conscious dogs prepared by surgical bladder division. Two types of experiments were made : A. maximal water diuresis, and B. Total blockade of distal NaCl reabsorption with ethacrynic acid and chlorothiazide. In maximal water diuresis CH2O + CNa was used as a measure of fluid delivery to the distal nephron. At similar GFR on both sides, the proximal reabsorption estimated as GFR--(CH2O + CNa) was 38.4 +/- 5.6 ml/min for the intact and 35.9 +/- 4.2 ml/min for the denervated kidney (n = 6, difference NS). After distal tubular blockade, proximal Na+ reabsorption calculated as filtered load minus urinary excretion was 3.84 +/- 0.43 mmol/min for the intact and 3.91 +/- 0.36 mmol/min for the denervated kidney (n = 6, difference NS). The fractional reabsorption of NA+ was 64.9 +/- 1.0% for the intact and 66.9 +/- 1.1% for the denervated kidney (difference NS). In contrast to data from renal denervation studies with anaesthetized animals, the present experiments did not show any difference in proximal reabsorption between the innervated- and denervated kidney. We conclude that in absence of anaesthesia renal efferent nerves have no major effect on NaCl transport in dog proximal tubule.

Animals↗
PubMed2000

Comparative metabolism and excretion of benzo(a)pyrene in 2 species of ictalurid catfish.

Differential susceptibility of polycyclic aromatic hydrocarbon (PAH)-mediated liver cancer exists in two related species of Ictalurid catfish. Two hypotheses are addressed in this study to explain this difference. Specifically, the relatively insensitive channel catfish 1) do not produce mutagenic PAH metabolites, and/or 2) they more quickly eliminate PAHs due to greater Phase II enzyme activities than the more sensitive brown bullhead. Livers and bile were collected from each species 6, 24, 72, and 168 h after a single 10 mg/kg i.p. benzo(a)pyrene (BaP) exposure. BaP treatment had no significant effect on cytosolic 1-chloro-2,4-dinitrobenzene or ethacrynic acid (EA)-glutathione-S:- transferase (GST) and cis-stilbene oxide-microsomal epoxide hydrolase (EH) activities of either species. Channel catfish EH and GST activities were 1.2-fold higher than brown bullhead activities (p = 0.058 and p < 0.002, respectively). HPLC-APCI-MS of extracted bile and bile enzymatically digested to detect glucuronyl transferase (GT), GST, and sulfotransferase (ST) conjugated metabolites indicated no species differences in elimination or profiles of total biliary metabolites. GT conjugates predominated; ST and GST conjugates were minimal. BaP-diones accounted for the majority of metabolites in both species. Overall, these results indicated that brown bullhead preferentially formed BaP-7,8-dihydrodiol, a precursor to the DNA-reactive BaP-7, 8-dihydrodiol-9,10-epoxide (BPDE), which may be linked to the increased PAH susceptibility in this species.

Animals↗
PubMed1975

Diuretics: mechanism of action and clinical application.

Despite the bewildering number of diuretics available to the physician, these drugs can be divided into 4 main groups, characterised by their site of action on sodium reabsorption in the kidney. Drugs acting on the ascending limb of the loop of Henle have a powerful but short acting diuretic effect; they include frusemide, ethacrynic acid and bumetanide. The benzothiadiazines and related compounds have a moderate diuretic action spread over a longer period, whilst the potassium-sparing diuretics, triamterene, amiloride and spironolactone, have only a weak diuretic effect but a marked ability to diminish urinary potassium excretion. The fourth group is made up of miscellaneous substances which function as vasodilator or osmotic agents. The pathogenesis of oedema formation in heart failure is outlined and a logical approach to treatment suggested. Duiretics are being increasingly used in the treatment of non-oedematous states, in particular hypertension, diabetes insipidus and hypercalciuria; their exact role in pregnancy and acute renal failure remains controversial. Side-effects can be related to their effect on electrolyte excretion and include hypokalaemia, hyponatraemia, hyperkalaemia and hyperuricaemia. The incidence of disturbed carbohydrate tolerance in previously normal individuals is low. Other less common side-effects are also discussed.

Acute Kidney Injury↗
PubMed1990

Cellular recovery of glyceraldehyde-3-phosphate dehydrogenase activity and thiol status after exposure to hydroperoxides.

The activity of the thiol-dependent enzyme glyceraldehyde-3-phosphate dehydrogenase (GPD), in vertebrate cells, was modulated by a change in the intracellular thiol:disulfide redox status. Human lung carcinoma cells (A549) were incubated with 1-120 mM H2O2, 1-120 mM t-butyl hydroperoxide, 1-6 mM ethacrynic acid, or 0.1-10 mM N-ethylmaleimide for 5 min. Loss of reduced protein thiols, as measured by binding of the thiol reagent iodoacetic acid to GPD, and loss of GPD enzymatic activity occurred in a dose-dependent manner. Incubation of the cells, following oxidative treatment, in saline for 30 min or with 20 mM dithiothreitol (DTT) partially reversed both changes in GPD. The enzymatic recovery of GPD activity was observed either without addition of thiols to the medium or by incubation of a sonicated cell mixture with 2 mM cysteine, cystine, cysteamine, or glutathione (GSH); GSSG had no effect. Treatment of cells with buthionine sulfoximine (BSO) to decrease cellular GSH by varying amounts caused a dose-related increase in sensitivity of GPD activity to inactivation by H2O2 and decreased cellular ability for subsequent recovery. GPD responded in a similar fashion with oxidative treatment of another lung carcinoma cell line (A427) as well as normal lung tissue from human and rat. These findings indicate that the cellular thiol redox status can be important in determining GPD enzymatic activity.

Cell Line↗
PubMed1979

Renal metabolic rate during changes in bicarbonate-dependent sodium reabsorption in the proximal tubules.

Previous studies indicate that water and at least 2 mol NaCl are reabsorbed in the proximal tubules for each mol NaHCO3 reabsorbed. To examine the effect on cortical energy metabolism of variations in this bicarbonate-dependent sodium reabsorption, the cortical metabolic rate was examined in anaesthetized dogs by the heat production technique during continuous infusion of saline and ethacrynic acid. Sodium reabsorption was altered either by intravenous infusion of a large dose of acetazolamide (500 mg/kg body wt) or by changing plasma Pco2 during metabolic alkalosis. Acetazolamide reduced bicarbonate reabsorption by 71 +/- 2%, sodium reabsorption by 54 +/- 2% and cortical heat production by 21 +/- 3%. A rise in Pco2 to 16.4 +/- 1.3 kPa during metabolic alkalosis increased sodium reabsorption by 25 +/- 3% and cortical heat production by 14 +/- 2%. A similar elevation of plasma Pco2 during metabolic acidosis had no effect on electrolyte reabsorption or the cortical metabolic rate. A reduction in Pco2 to 2.3 +/- 0.3 kPa reduced sodium reabsorption by 40 +/- 3% and cortical heat production by 19 +/- 2%. We conclude that a rise in proximal tubular reabsorption requires energy. However, the changes in energy requirement are small, accounting for previous failures to observe significant changes in cortical energy metabolism during less extensive changes of sodium reabsorption in the proximal tubules.

Acetazolamide↗
PubMed2001

Differential induction of glutathione S-transferases in the clam Ruditapes decussatus exposed to organic compounds.

Studies of glutathione S-transferase (GST) induction were performed in the Mediterranean clam Ruditapes decussatus after controlled exposure to organics in holding tanks. Clams were treated with phenobarbital (PB), benzo[a]pyrene (BaP), and 2,2-bis-(p-chlorophenyl)-1,1-dichlorethylene (p,p'-DDE). Three different substrates, i.e., 1-chloro-2,4-dinitrobenzene (CDNB), ethacrynic acid (ETHA), and paranitrobenzene chloride (PNBC), were used to determine GST activities in order to distinguish the isoenzymes induced by contamination. The isoforms conjugating ETHA were significantly induced by treatment with PB and BaP, whereas exposure to p,p'-DDE induced isoforms conjugating CDNB and ETHA. An antibody against affinity-purified GSTs from R. decussatus was prepared by injection into rabbit. The serum containing the antibody gave a positive reaction with both the purified GSTs from R. decussatus and the low molecular weight GSTs from rat. Subcellular fractions from both control and treated animals were analyzed by Western blot. Cytosolic extracts from clams contaminated with PB and p,p'-DDE showed a 24-kDa band in addition to the 26-kDa band recognized by the antibody. Results of these studies suggest that, in R. decussatus, organics may induce GSTs belonging to the pi class.

Animals↗
PubMed1993

Chronic electrical stimulation reverses deafness-related depression of electrically evoked 2-deoxyglucose activity in the guinea pig inferior colliculus.

The [14C]-2-deoxyglucose (2-DG) autoradiographic technique was used to study how auditory-related metabolic activity changes with deafness, and how chronic electrical stimulation of the deafened system may modify these changes. Guinea pigs were deafened by administration of kanamycin and ethacrynic acid. After nine weeks of deafness, the basal unstimulated uptake of 2-DG in the inferior colliculus (IC) was lower than in normal hearing control animals. 100 microA of acute cochlear electrical stimulation significantly increased 2-DG uptake in normal hearing animals but did not evoke a significant increase in four or nine week deafened animals. Electrically elicited 2-DG uptake in the IC is therefore depressed by prolonged deafness. In a second series of experiments, after four weeks of deafness, animals were chronically electrically stimulated via a cochlear implant 2.5-3.5 h a day, five days a week for five weeks at 100 microA. Acute cochlear electrical stimulation following this chronic stimulation significantly increased 2-DG uptake in the contralateral IC over unstimulated levels. This suggests that some depressive effects of profound deafness on the auditory brain stem may be reduced or reversed with chronic electrical stimulation by a cochlear implant.

Animals↗
PubMed1993

Combined effects of cadmium and nickel on hepatic glutathione S-transferases in rats.

1. The acute combined effects of cadmium (Cd) and nickel (Ni) on rat hepatic glutathione S-transferase (GST) activities toward the substrates 1-chloro-2,4-dinitrobenzene (CDNB), 1,2-dichloro-4-nitrobenzene (DCNB) and ethacrynic acid (EAA) were determined and compared to those of Cd or Ni alone. 2. Male adult rats (225-275 g) were administered either a single dose of Cd (3.58 mg CdCl2.H2O/kg, i.p.) 72 hr prior to sacrifice or a single dose of Ni (59.5 mg NiCl2.6H2O/kg, s.c.) 16 hr prior to sacrifice. For the combined treatment, animals received the single dose of Ni 56 hr after the single dose of Cd and they were killed 16 hr later. 3. Cd treatment alone did not produce any changes in the hepatic GST activities toward the substrates studied. 4. Ni treatment alone, however, significantly increased hepatic GST activity toward EAA whereas it was ineffective on GST activities for CDNB and DCNB. 5. Combined treatment of metals did not alter hepatic GST activities toward the substrates CDNB and DCNB. Hepatic GST activity for EAA, however, was significantly increased by the combined treatment. Nevertheless, the combined treatment did not augment the increase in GST activity for EAA noted by Ni treatment alone.

Animals↗
PubMed2001

Induction of glutathione S-transferase activity and protein expression in brown bullhead (Ameiurus nebulosus) liver by ethoxyquin.

The inducibility of hepatic cytosolic glutathione S-transferases (GSTs) was examined in brown bullheads, a freshwater fish that is highly susceptible to hepatic neoplasia following exposure to carcinogen-contaminated sediments. Juvenile bullheads were fed a semi-purified antioxidant-free diet supplemented with ethoxyquin (0.5% w/w dissolved in 3% corn oil), a prototypical rodent GST-inducing agent, twice daily for 14 days. Control bullheads received the antioxidant-free diet supplemented with corn oil (3% w/w). A significant increase (1.6-fold, p < or = 0.01) in hepatic cytosolic GST activity toward 1-chloro-2,4-dinitrobenzene (CDNB) was observed in the ethoxyquin-treated bullheads relative to control fish. A trend toward increased GST-NBC activity was observed in the ethoxyquin-treated fish (1.2-fold, p = 0.06), whereas no treatment-related effects were observed on GST activities toward ethacrynic acid (ECA). In contrast, GST activity toward (+/-)-anti-benzo[a]pyrene-trans-7,8-dihydrodiol-9,10-epoxide (BPDE) was repressed in affinity-purified cytosolic fractions prepared from ethoxyquin-treated bullheads relative to control bullheads. Silver staining and densitometric analysis of isoelectric-focused, affinity-purified GST proteins revealed increased expression of two basic GST-like isoforms in ethoxyquin-treated fish. In summary, exposure to ethoxyquin increases brown bullhead GST-CDNB catalytic activity and hepatic cationic GST protein expression. However, the increase in overall GST-CDNB activity by ethoxyquin is associated with repression of GST-BPDE activity, suggesting differential effects on hepatic bullhead GST isoforms by ethoxyquin. The potential repression of bullhead GST isoforms that conjugate the carcinogenic metabolites of PAH metabolism under conditions of environmental chemical exposure could be a contributing factor in the sensitivity of bullheads to pollutant-associated neoplasia.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed1994

Mitomycin C sensitivity in human bladder cancer cells: possible role of glutathione and glutathione transferase in resistance.

In this study, we have examined the relationship between sensitivity to mitomycin C (MMC) and glutathione (GSH) and glutathione transferase (GST) levels using a panel of three unrelated human bladder cancer cell lines. J82, HT-1197, and SCaBER. Cell lines HT-1197 and SCaBER were about 2- and 4.5-fold more resistant to MMC as compared to J82. Although the GSH level did not differ significantly in these cell lines, GST activity in HT-1197 and SCaBER cells were higher by about 2.3- and 6.0-fold, respectively, as compared to J82. Similar to GST activity, GST pi content was highest in the most insensitive cell line and lowest in J82 cells. The cytotoxicity of MMC was increased significantly in these cells by a 1-h pretreatment with a nontoxic concentration of ethacrynic acid (EA), an inhibitor of GST activity. EA pretreatment resulted in a marked GSH depletion as well as GST activity inhibition in both of these cells. Although pretreatment of J82 and SCaBER cells with a nontoxic concentration of D,L-buthionine-S,R-sulfoximine (BSO) caused similar GSH depletion, the cytotoxicity of MMC was enhanced only in SCaBER cells. The differential effect of BSO on MMC cytotoxicity in these cell lines appeared to be due to the differences in the extent of GSH regeneration after removal of BSO. While a marked GSH regeneration occurred in J82 cells within 1 h after BSO removal, such an effect was not observed in SCaBER cells. Combined treatment of these cells with BSO and EA produced a greater potentiation of MMC cytotoxicity in both the cell lines when compared to BSO or EA treatment alone. We conclude that GSH/GST levels may affect the sensitivity of human bladder cancer cells to MMC.

Antimetabolites, Antineoplastic↗
PubMed1999

Discontinuities in the temperature function of transmembrane water transport in Chara: relation to ion transport.

The NMR (nuclear magnetic resonance) method of Conlon and Outhred (1972) was used to measure diffusional water permeability of the nodal cells of the green alga Chara gymnophylla. Two local minima at 15 and 30 degreesC of diffusional water permeability (Pd) were observed delimiting a region of low activation energy (Ea around 20 kJ/mol) indicative of an optimal temperature region for membrane transport processes. Above and below this region water transport was of a different type with high Ea (about 70 kJ/mol). The triphasic temperature dependence of the water transport suggested a channel-mediated transport at 15-30 degreesC and lipid matrix-mediated transport beyond this region. The K+ channel inhibitor, tetraethylammonium as well as the Cl- channel inhibitor, ethacrynic acid, diminished Pd in the intermediate temperature region by 54 and 40%, respectively. The sulfhydryl agent p-(chloromercuri-benzensulfonate) the water transport inhibitor in erythrocytes also known to affect K+ transport in Chara, only increased Pd below 15 degreesC. In high external potassium ('K-state') water transport minima were pronounced. The role of K+ channels as sensors of the optimal temperature limits was further emphasized by showing a similar triphasic temperature dependence of the conductance of a single K+ channel also known to cotransport water, which originated from cytoplasmic droplets (putatively tonoplast) of C. gymnophylla. The minimum of K+ single channel conductance at around 15 degreesC, unlike the one at 30 degreesC, was sensitive to changes of growth temperature underlining membrane lipid involvement. The additional role of intracellular (membrane?) water in the generation of discontinuities in the above thermal functions was suggested by an Arrhenius plot of the cellular water relaxation rate which showed breaks at 13 and 29 degreesC.

4-Chloromercuribenzenesulfonate↗
PubMed1992

Potentiation by thiopurines and sulfhydryl-reactive agents of the inhibition by 3-deazaadenosine of mononuclear phagocytes.

Combination effects of 3-deazaadenosine (c3Ado) on antibody-dependent phagocytosis in mouse resident peritoneal cells and human peripheral blood monocytes precultured with cytotoxic thiols, azathioprine (AZA) or 6-mercaptopurine (6-MP), and thiol-reactive agents, 2-cyclohexene-1-one (2-CH) or ethacrynic acid (ETA), are described. In the mouse cell preparations, a non-inhibitory concentration of 10 microM AZA or 6-MP potentiated the inhibition by 5 and 10 microM c3Ado of phagocytosis. Higher concentrations of AZA or 6-MP (50, 100 microM) and c3Ado (40, 50 microM) were needed to achieve similar effects in human monocytes. Both 2-CH (50 microM) and ETA (25 microM) inhibited mouse cell phagocytosis and acted synergistically with c3Ado. Precultivation of mouse cells with an inhibitor of glutathione synthesis, buthionine sulfoximine (BSO, 50 microM) caused no inhibition of phagocytosis and no potentiation of the inhibition by c3Ado, although BSO potentiated the inhibition by 2-CH (50 microM). In human monocytes, non-inhibitory concentrations (10 and 25 microM) of gold sodium thiomalate (GST), AZA, and c3Ado, but not 6-MP, potentiated the inhibition by 2-CH (25-37.5 microM) of phagocytosis. Results are discussed in connection with the possible modulation by endogenous sulfhydryl-reactive metabolites of phospholipid turnover of the effects of c3Ado.

Animals↗