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PubMed1985

Metabolism of pantethine in cystinosis.

D-Pantethine is a conjugate of the vitamin pantothenic acid and the low-molecular-weight aminothiol cysteamine. Pantethine is an experimental hypolipemic agent and has been suggested as a source of cysteamine in the treatment of nephropathic cystinosis. We treated four cystinotic children with 70-1,000 mg/kg per d oral D-pantethine and studied its metabolism. Pantethine was rapidly hydrolyzed to pantothenic acid and cysteamine; we could not detect pantethine in plasma after oral administration. The responsible enzyme, "pantetheinase," was highly active in homogenates of small intestinal mucosa and plasma. The Michaelis constant of the rat intestinal enzyme was 4.6 microM and its pH profile showed a broad plateau between 4 and 9. Pantothenate pharmacokinetics after orally administered pantethine followed an open two-compartment model with slow vitamin elimination (t1/2 = 28 h). Peak plasma pantothenate occurred at 2.5 h and levels over 250 microM were seen at 300 times normal. Apparent total body storage of pantothenate was significant (25 mg/kg), and plasma levels were elevated threefold for months after pantethine therapy. Plasma cysteamine concentrations after pantethine were similar to those reported after equivalent doses of cysteamine. However, at best only 80% white blood cell cystine depletion occurred. We conclude that pantethine is probably less effective than cysteamine in the treatment of nephropathic cystinosis and should only be considered in cases of cysteamine intolerance. Serum cholesterol was decreased an average of 14%, which supports the potential clinical significance of pantethine as a hypolipemic agent. Rapid in vivo hydrolysis of pantethine suggests that pantothenate or cysteamine may be the effectors of its hypolipemic action.

Adolescent↗
PubMed1995

Recent advances in the treatment of cystinosis.

Cysteamine bitartrate capsules (Cystagon) have been approved by the US Food and Drug Administration for use in patients with nephropathic cystinosis. Plasma cysteamine concentrations were virtually identical at various times following ingestion of either cysteamine hydrochloride or Cystagon capsules in 24 normal control subjects. A transfer study was done with eight cystinosis patients who had been receiving either cysteamine hydrochloride or phosphocysteamine for many years. The plasma cysteamine concentration was significantly higher 2h after Cystagon and the leukocyte cystine content was significantly lower at all times after Cystagon compared to older forms of the drug. These differences are probably the result of greater patient compliance in taking the capsules compared to the older, liquid forms of the drug. A new method for following the course of renal glomerular deterioration in diseases such as cystinosis has been published recently. This method was used to re-analyse data on the efficacy of cysteamine treatment and to re-analyse new data on treating cystinosis patients with either of two doses of cysteamine (1.30 g/m2 per day and 1.95 g/m2 per day). This new method agrees well with other methods and shows that both doses of drug are equally effective in maintaining glomerular function.

Adolescent↗
PubMed1999

Dual effect of female sex steroids on drug-induced gastroduodenal ulcers in the rat.

Since the sexual dimorphism of gastroduodenal ulcers is well known and might possibly relate to the actions of sex hormones, we studied the role of the female sex steroids, progesterone and 17beta-estradiol in cysteamine-induced mucosal ulcers in female Wistar rats (200-220 g). Administration of cysteamine (400 mg/kg, s.c.) provoked macroscopic gastroduodenal mucosa injury as assessed planimetrically, an increase in microvascular permeability in the stomach and the duodenum as assessed by extravasation of radiolabelled albumin, and decreased gastroduodenal mucus levels as assessed by the Alcian blue technique. Ovariectomy (2 weeks before cysteamine) decreased plasma 17beta-estradiol level as assessed by radioimmunoassay, gastroduodenal macroscopic injury and albumin extravasation, and increased mucus levels following cysteamine challenge. Administration of progesterone (10-50 mg/kg/week, s.c.) attenuated in a dose-dependent manner cysteamine-induced gastroduodenal mucosa injury and microvascular leakage, while it increased mucus levels in the stomach and the duodenum. In contrast, administration of 17beta-estradiol (1-5 mg/kg/week, s.c.) dose-dependently augmented gastric and duodenal macroscopic mucosa lesions and microvascular injury provoked by cysteamine, and caused a further reduction in gastroduodenal mucus levels observed after cysteamine administration. In different experiments, ovariectomy decreased indomethacin-induced gastroduodenal injury. The injection of 17beta-estradiol (1-5 mg/kg/week) did not affect gastroduodenal damage, while treatment with progesterone (10-50 mg/kg/week) protected against indomethacin-provoked mucosa ulcers. It is concluded that female sex steroids play a role in drug-induced gastroduodenal ulcers by modulating microvascular permeability and mucus secretion.

Animals↗
PubMed1985

Biliary and pancreatic secretions influence experimental duodenal ulcer without affecting gastric secretion in the rat.

The effect of the absence of biliary and/or pancreatic secretions in the duodenum or the enhanced presence of bile at the proximal duodenum on the incidence, severity, number, and location of cysteamine-induced duodenal ulcers was investigated in the rat. Cysteamine produced ulcers on the anterior wall of the duodenum in 75% and on the posterior wall ("kissing ulcers") in 50% of the animals. Diversion of biliary and/or pancreatic secretions from the duodenum increased both the severity and the incidence of the posterior duodenal ulcers. Diversion of bile to the proximal duodenum, on the other hand, decreased the severity as well as the incidence of the anterior duodenal ulcers. Mortality in rats receiving cysteamine correlated with the severity of ulcers. Taurocholic acid at nontoxic doses given subcutaneously or orally to nonoperated rats and rats which had bile diverted to the proximal duodenum aggravated the cysteamine-caused duodenal ulcers. Neither proximal nor distal diversion of bile had a major effect on gastric secretion of acid and pepsin in normal or cysteamine-treated rats. We conclude that both bile and pancreatic secretions may directly influence the development of cysteamine-induced duodenal ulcers in the rat.

Animals↗
PubMedDate not supplied

Effects of somatostatin deficiency on cell distribution within the Langerhans islets.

Insulin, glucagon and somatostatin (SLI) in the pancreas and the gastrointestinal tissue of rats were measured following a high (300 mg/kg) or low (150 mg/kg) dose of cysteamine, given intermittently for 14 days. In addition, the effect of prolonged cysteamine-induced depletion of pancreatic SLI upon the cell distribution within the Langerhans islets was compared with that of chronic insulin-deficient rats produced by streptozotocin. The high or low dose of cysteamine reduced pancreatic SLI to 8.3% and gastrointestinal SLI to 5.6% of control levels without duodenal ulcer. The high dose of cysteamine also reduced pancreatic insulin to 37% of controls without hyperglycemia. No change in the glucagon concentration was observed. In SLI-deficient rats, distribution of A and B cells was similar to that of controls, even though D cells were rarely seen. In insulin-deficient rats, however, the number of A and D cells per islet area increased with a concomitant decrease in B cells. Intermittent administration of a low dose of cysteamine, thus, appears to be useful to produce a chronic SLI-deficient rat. However, a high dose of cysteamine is not a specific depletor of pancreatic SLI. Although insulin may be important to maintain normal cell distribution within the islets, pancreatic SLI may not have such a role.

Animals↗
PubMed1976

In vitro evaluation of some latent radioprotective compounds.

In tissue culture, protection against X-irradiation by a number of cysteamine derivatives was studied and the results were compared with data obtained in mice. Compounds with a covered SH group, like WR 638, cysteamine phosphate, WR 2721, and AE 48527, showed practically no protection when dissolved in tissue-culture medium, but developed a protective activity when dissolved in rat blood. Thiol measurements demonstrated that in rat blood the compounds were partly hydrolysed to thiols. C511 was also hydrolysed in culture medium and was slightly less effective than cysteamine in culture medium. Cysteamine phosphate was hydrolsed more easily than cysteamine sulphate and the protective activity in rat blood was better. WR 2721 was also partly hydrolysed in rat blood. The in vitro protection of this compound was disappointing when compared with results in vivo. Its SH form (WR 1065) also showed less protection than expected from in vivo experiments. Thus, the little protection by WR 2721 in vitro in rat blood is not only due to its incomplete conversion into its thiol. Longer incubation times and the use of rat blood as a solvent brought the protective activity of WR 1065 almost up to the level of cysteamine. This may indicate that WR 1065 penetrates the cells poorly. WR 1065 was the only compound we studied whose protective activity in vitro was improved appreciably by dissolving it in rat plasma.

Amifostine↗
PubMed1989

[Effects of furazolidone on brain monoamines in the treatment of peptic ulcer].

The purpose of this study was to investigate the protective role of furazolidone against the formation of duodenal ulcer induced by cysteamine and the effect of furazolidone on NE, DA and 5-HT concentrations in various brain regions (telencephalon, diencephalon and brainstem). The results indicated that one dose of cysteamine (280 mg/kg) produced 90-92% ulceration with no mortality within the first 24 hours, whereas cysteamine plus furazolidone significantly decreased the duodenal ulceration from 90% to 0. Using a sensitive spectrofluorimetric method, we found that cysteamine markedly diminished the NE levels in all regions but the DA level only in telencephalon. Meanwhile, cysteamine plus furazolidone increased the DA level in the same region. This suggested that the protective role of furazolidone against the formation of duodenal ulcer induced by cysteamine in rat may be related to increased DA level in telencephalon.

Animals↗
PubMed1984

Normalization of receptor binding of apolipoprotein E2. Evidence for modulation of the binding site conformation.

Apolipoprotein (apo-) E3, when combined with the phospholipid dimyristoylphosphatidylcholine (DMPC), binds avidly to apo-B,E (low density lipoprotein) receptors on human fibroblasts. Apolipoprotein E2 isolated from type III hyperlipoproteinemic subjects, which differs from apo-E3 by the presence of cysteine instead of arginine at residue 158, possesses only about 1% of the receptor binding activity of apo-E3. Modification of apo-E2 with cysteamine, which converts the cysteine at position 158 to a positively charged lysine analogue, activates receptor binding approximately 13-fold. In the present experiments, thrombin was used to cleave apo-E2 into two fragments (Mr = 22,000 and Mr = 10,000). The larger fragment, which has been shown to possess the receptor binding domain, displayed binding activity up to 12-fold greater than intact apo-E2 or equivalent to apo-E2 treated with cysteamine. When the Mr = 22,000 fragment was modified with cysteamine and combined with DMPC, receptor binding was further enhanced, attaining the level of activity of normal apo-E3 X DMPC, a 100-fold increase over apo-E2 X DMPC binding. When the cysteamine modification was reversed by incubation with beta-mercaptoethanol, the Mr = 22,000 fragment retained most of its binding activity. However, when the same sample was tested 24 h later, the level of binding activity dropped significantly. The receptor binding of apo-E2-containing beta-very low density lipoproteins could also be activated by cysteamine treatment, with the same retention of enhanced binding activity occurring after the reversal of the modification. These results indicate that apo-E2 can attain full binding activity by the removal of the carboxyl-terminal one-third of the molecule and the addition of a positive charge at residue 158 of the molecule. The retention of enhanced binding after the reversal of the cysteamine modification indicates that the enhanced binding is probably due to conformational changes induced in the binding domain (and maintained by the phospholipid) and not merely to the presence of the positive charge at residue 158.

Apolipoprotein E2↗
PubMed1980

Regulatory role of glutathione and soluble sulfhydryl groups in the toxicity of adriamycin.

Adriamycin (ADR) has been shown to produce free radicals in NADPH microsomal systems, to increase oxygen consumption of both hepatic microsomes and heart sarcosomes and to stimulate superoxide formation in cardiac, submitochondria particles. These reactive products could produce the cardiotoxicity of ADR by oxidizing various membrane structures, especially if the heart lacks sufficient protective reducing substances such as thiols. We examined 1) the effect of ADR on reduced glutathione (G-SH) levels in various tissues including heart, 2) the ability of the sulfhydryl (SH) donor, cysteamine, to alter soluble SH levels in heart tissue after ADR administration and 3) the effects of SH donors (cysteamine and N-acetyl cysteine and G-SH depletion by diethyl maleate on ADR-induced lethality in Swiss ICR-HA mice. A single injection of ADR (15 mg/kg i.p.) elicited a statistically significant fall in liver (P < .05), heart (P < .02) and erythrocyte (P < .01) G-SH levels. Treatment with cysteamine protected against the fall in soluble SH groups in heart tissue. Cysteamine (50 mg/kg, i.p., every 8 hr for 6 days) or N-acetylcysteine (100 mg/kg, i.p., 1 hr before and 7 hr after ADR) protected against ADR-induced lethality and decreased the appearance of microscopic myocardial lesions. When endogenous levels of G-SH were depleted by diethyl maleate (300 mg/kg i.p., every 8 hr for 4 days), ADR lethality was markedly potentiated. Diethyl maleate alone did not cause death. We conclude 1) ADR significantly lowers G-SH levels in erythrocytes, liver and heart tissue, 2) the lowering of cardiac SH groups by ADR can be prevented by cysteamine and 3) ADR toxicity can be potentiated by diethyl maleate, a G-SH depletor, and reduced by cysteamine or N-acetyl cysteine, SH donors. These results suggest that the G-SH system may be involved in the modulation of ADR-induced toxicity.

Animals↗
PubMed1995

Uptake and subcellular distribution of 51Cr in Gomori-positive astrocytes in primary culture.

An unusual population of astrocytes containing Gomori-positive inclusions occurs in periventricular regions of the brain in all mammalian species. The inclusions are autofluorescent and exhibit non-enzymatic peroxidase activity. Estradiol treatment in vivo and cysteamine treatment in vitro have been shown to increase the number and size of these inclusions. Recent studies indicate that the Gomori inclusions are accumulations of autophagocytized abnormal mitochondria. The mitochondrial changes initiating Gomori inclusion formation begin with a loss of cristae. Energy dispersive X-ray microanalysis also reveals small emission peaks indicative of chromium. The appearance of chromium peaks in the initial stages of mitochondrial transformation suggests that enhanced permeability to chromium could play a causal role in generating Gomori inclusions. In the present study, we have examined the uptake and intracellular distribution of chromium during Gomori inclusion formation in cysteamine-treated cultured astrocytes. 51Cr was added to the media of glial cultures 24 hours prior to the initiation of the formation of Gomori inclusions by the addition of cysteamine. Cultures were fixed and prepared for EM radioautography at 12, 24, and 72 hours following the addition of cysteamine. 51Cr was added to control cells but they were not treated with cysteamine, and, they did not, therefore, develop Gomori inclusions. Cysteamine exposure resulted in a rapid sustained increase in radiolabel over the astrocytes. Much of the label was concentrated over mitochondria. At the late time points, label concentrated progressively over developing Gomori inclusions. These results confirm that the onset of Gomori inclusion formation coincides with increase cellular permeability to chromium and they indicate that uptake of chromium by mitochondria may play an important role in initiating development of these structures.

Animals↗
PubMed1996

Stimulation of glutathione synthesis of in vitro matured bovine oocytes and its effect on embryo development and freezability.

Glutathione (GSH) has been shown to play an important role in embryo development. In a previous study, we demonstrated that cysteamine supplementation of in vitro maturation (IVM) medium increased the intracellular GSH content in bovine oocytes and improved subsequent embryo development to the blastocyst stage. The present study was carried out to evaluate the effect of inhibition by buthionine sulfoximide (BSO) of GSH synthesis during IVM in the presence of cysteamine, on subsequent embryo development, and the effect of cysteamine during IVM on the survival of blastocysts following freezing. The effect of beta-mercaptoethanol and cysteine added to the maturation medium on GSH levels in bovine oocytes, as well as the effect of these compounds on de novo GSH synthesis by oocytes during in vitro maturation, was also studied. The inhibitory effect of BSO during in vitro maturation on GSH synthesis was also evaluated. Evidence was found confirming that GSH synthesis occurs intracellularly during IVM of oocytes and is stimulated by cysteamine, beta-mercaptoethanol and cysteine. Moreover, the present results suggest that the increase in the rate of embryo development exerted by cysteamine, when present during IVM, was due to its stimulatory effect on GSH synthesis. This increase in GSH levels during IVM improves embryo development and quality, producing more embryos reaching the blastocyst stage on day 6, those most suitable for freezing.

Animals↗
PubMed2006

Glutathione content and glutathione peroxidase expression in in vivo and in vitro matured equine oocytes.

The in vitro developmental competence of equine oocytes is still low in comparison with other domestic mammals. A major factor affecting the viability of cells during in vitro culture is the increased oxidative stress. Oxidative modifications could be responsible for oocyte incompetence for in vitro maturation (IVM). Cysteamine, a glutathione (GSH) synthesis enhancer, has been shown to increase intracellular GSH content and to improve embryo development when added during IVM of bovine, porcine, and ovine oocytes. The aim of the present study was (1) to determine whether equine cumulus-oocyte complexes (COCs) benefit from the addition of cysteamine during IVM, (2) to compare the GSH content of oocytes after in vivo maturation and IVM, (3) to assess whether cysteamine administration during IVM of equine oocyte enhances early embryonic developmental capability following ICSI, (4) to study the glutathione peroxidase (GPX) mRNA level in COCs. In vivo matured COCs were collected by aspiration from preovulatory follicles, and analyzed at collection. Immature COCs were collected in vivo or from slaughterhouse ovaries and matured in culture media supplemented or not with 100 microM cysteamine. After nuclear stage assessment, oocytes were analyzed for GSH concentration and both oocytes and cumulus cells were analyzed for GPX and GAPDH mRNA. Our data showed that the maturation capability was similar in both in vivo aspirated oocytes and in those isolated from slaughterhouse ovaries. Moreover, the addition of cysteamine during IVM affected neither GSH content nor maturation rate. At the time of collection, intra-oocyte GSH content was not influenced by the chromatin status. GSH concentration was similar in in vivo and in vitro matured metaphase II (MII) stage oocytes, and was significantly higher in MII than immature germinal vesicle stage oocytes. Moreover, the presence of serum inhibited whereas its absence stimulated the accumulation of GSH within oocytes during IVM. After ICSI, a similar proportion of zygotes in each group developed beyond the two-cell stage after 72 hr of culture. Cumulus cells expressed GPX mRNA, while GPX transcript was absent in both immature and mature oocytes. Cumulus expression of GPX mRNA was significantly higher when analyzed at collection than after IVM. Taken together, our results demonstrate that in equine oocytes, GSH increases during IVM but the relative intra-oocyte content of this thiol does not affect maturation and early development efficiency after fertilization. We hypothesize that factor(s) other than GSH/GPX are responsible for the limited in vitro early developmental capability of equine oocytes.

Animals↗
PubMed1991

Decrease of duodenal calcitonin gene-related peptide- and substance P-like immunoreactivity in rat duodenal ulcers.

We have investigated the endogenous levels of duodenal calcitonin gene-related peptide- (CGRP) and Substance P- (SP) like immunoreactivity (li) following the induction of duodenal ulcers in rats. Using three duodenal ulcerogens, namely cysteamine, dulcerozine or mepirizole given in a single oral dose, a decrease of duodenal CGRP-li and SP-li was observed. Time-relationship studies of this phenomenon show that CGRP-li and SP-li were decreased concomitantly to the formation of gastroduodenal ulcers after the administration of cysteamine (900 mg/kg p.o.). Pretreatment with the selective sensory neurotoxin capsaicin induced CGRP-li decrease in the duodenum, which was not further decreased by an ulcerogenic dose of cysteamine, indicating that cysteamine induced a release of CGRP-li of capsaicin-sensitive origin. Otherwise duodenal SP-li was not sensitive to capsaicin pretreatment and its duodenal content decreased by cysteamine originates from an intrinsic source. Our observations indicate that CGRP and SP may play an important local role in duodenal ulcerogenesis.

Animals↗
PubMed1998

Precursors of taurine in female genital tract: effects on developmental capacity of bovine embryo produced in vitro.

Two precursors of taurine have been studied: cysteamine and hypotaurine. Cysteamine has been quantified in genital secretions and found in follicular fluids of all species tested. On the contrary cysteamine was not detected (or traces) in tubal fluids of the same species. Addition of 50, 100 or 250 microM of cysteamine to the maturation medium used in the culturing of bovine oocytes did not improve the cleavage rate nor the embryo's developmental potential in vitro. Furthermore, at 250 microM, cysteamine seems to be toxic to the embryo. Addition of 0.5-1 mM hypotaurine to the bovine embryo culture medium improved significantly blastocyst production and quality. The respective roles of these 2 taurine precursors on maturation and embryo development are discussed.

Animals↗
PubMed2005

A continuous spectrophotometric assay for human cystathionine beta-synthase.

We report a new continuous spectrophotometric assay for human cystathionine beta-synthase (hCBS). This assay relies upon the finding that hCBS will take cysteamine in place of L-homocysteine, thereby producing thialysine. Thialysine is, in turn, decarboxylated by lysine decarboxylase, releasing CO2 that is monitored by the sequential action of phosphoenolpyruvate carboxylase and L-malate dehydrogenase. The decrease in absorbance at 340 nm is monitored as reduced nicotinamide adenine dinucleotide is consumed. Using this four-enzyme couple, we find that Km(app) = 1.2+/-0.2 mM for L-serine and 5.6+/-2.2 mM for cysteamine, with kcat = 1.3+/-0.1s(-1) for the formation of thialysine by hCBS. For comparison purposes, the same hCBS reaction was monitored via a radioactive single time point assay using 14C-(C-1)-labeled L-serine and cysteamine as substrates, counting the thialysine product, following ion exchange chromatography. This assay yielded Km(app) = 2.2+/-0.5 mM for L-serine and 6.6+/-2.2 for cysteamine, with kcat = 2.5+/-0.4 s(-1). These numbers indicate that, although it possesses a shortened carbon chain and lacks a carboxyl group, cysteamine displays a catalytic efficiency (kcat/Km) with hCBS that is within an order of magnitude of that observed with its natural thiol cosubstrate, L-homocysteine.

Carboxy-Lyases↗
PubMed1991

DNA radiolysis by fast neutrons. II. Oxygen, thiols and ionic strength effects.

Plasmid DNA was irradiated with fast neutrons, and the protection by cysteamine against strand breakage (ssb and dsb) was evaluated in the presence and absence of oxygen. In the absence of cysteamine no radiosensitizing effect of oxygen was observed. In anoxia the protection factors, PF(ssb) and PF(dsb) of 1 mM cysteamine (in 50 mM potassium phosphate solution) were lower than the PFs observed with gamma-irradiation. The results agree with the radical repair model, in which the thiol competes with the oxygen produced inside the anoxic neutron-irradiated system, according to the 'oxygen-in-the-track' hypothesis. At low ionic strength in air-saturated solutions, positively charged cysteamine protects more efficiently than negatively charged thiolactate. The dependence of the PFs on the charge of the thiol can be explained by the condensation of counter-ions and depletion of co-ions around DNA, predicted by Manning's theory. Based on the same theory, we propose here an explanation of the ionic strength or by thiolactate at low ionic strength is largely due to scavenging of OH. radicals in the bulk solution. At low ionic strength the PF(ssb) of cysteamine is higher for neutrons than for gamma-irradiation. This might suggest different primary lesions for the two types of irradiation.

Cysteamine↗
PubMed2002

Follow-up and treatment of adults with cystinosis in the Netherlands.

BACKGROUND: Cystinosis is a rare autosomal recessive disease, caused by intracellular cystine accumulation due to a defect in the lysosomal cystine carrier. Treatment with cysteamine favours the transport of cystine out of the lysosomes, diminishes organ damage, and postpones the progression of renal failure. The extra-renal deposition of cystine continues after renal transplantation, leading to later complications. The objective of this study was to evaluate the follow-up, the occurrence of late complications, the social status, and the adequacy of cysteamine treatment in adult patients with cystinosis. METHODS: The medical histories of 10 adult cystinosis patients aged 19-36 years were studied. The impairment of thyroid function, central nervous system, endocrine pancreas, and ocular manifestations, as well as treatment with cysteamine were evaluated. RESULTS: Eight patients received in total 12 renal grafts, one patient was dialysed and one received conservative treatment for chronic renal failure. Extra-renal complications were noted in six patients, loss of visual acuity in four, hypothyroidism in three, diabetes mellitus in one, cerebral atrophy and epilepsy in one, and swallowing difficulties in two patients. Ophthalmic control was not performed in two patients, thyroid function was not controlled in two and glycaemia not controlled in two patients. Seven patients received 2100-4000 mg cysteamine per day in 2 (n=2), 3 (n=1), 4 (n=3), or 6 (n=1) doses. Cystine concentration in leukocytes was measured once or twice a year in eight patients and was within the recommended range only in three patients. CONCLUSION: A high rate of extra-renal complications in adults with nephropathic cystinosis was found. Optimizing the cysteamine therapy may attenuate these complications. Better communication between paediatric and 'adult's' nephrologists is needed to improve follow-up and treatment of grown-up cystinosis patients.

Adult↗
PubMed1997

Glutathione synthesis during in vitro maturation of bovine oocytes: role of cumulus cells.

Glutathione (GSH) synthesis during in vitro maturation (IVM) has been shown to play an important role in embryo development. The present study was carried out to evaluate the role of cumulus cells in GSH synthesis during IVM of bovine oocytes in the presence of cystine, cysteine, the cysteine analogue N-acetylcysteine, and cysteamine. For this purpose, cumulus-oocyte complexes (COCs), denuded oocytes (DOs), and DOs in coculture with a cumulus cell monolayer were used. An increase in GSH level stimulated by cystine was observed only in the presence of cumulus cells, either with COCs or in DOs matured on a coculture monolayer. Addition of cysteine and cysteamine to IVM medium increased GSH levels in COCs and DOs. N-Acetylcysteine increased GSH levels only in DOs. Moreover, cumulus cells contributed to the stimulatory effect exerted by cysteine and cysteamine on GSH synthesis in COCs. These results indicate that cumulus cells during IVM play an important role in oocyte GSH synthesis, allowing the oocytes to use cystine and contributing to the stimulatory effect exerted by cysteine and cysteamine. In addition, these results demonstrate that IVM medium supplemented with cysteine or cysteamine increased GSH content in oocytes without cumulus mass (DO) and in the absence of a cumulus cell monolayer. This may be useful to increase the efficacy of IVM of those oocytes having few cumulus cell layers, in a system without coculture.

Acetylcysteine↗