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At least 19 recordsLinked to original sources
PubMed1984

Effect of thioglycolate on phagocytic and microbicidal activities of peritoneal macrophages.

Brewer thioglycolate-elicited mouse peritoneal macrophages were as active as resident peritoneal macrophages in the phagocytosis of opsonized Staphylococcus epidermidis but were unable to kill ingested microorganisms. This decreased functional activity was restricted to Brewer thioglycolate-elicited macrophages, since peritoneal macrophages elicited with NIH thioglycolate, alone or supplemented with agar and methylene blue, were as active as resident peritoneal macrophages. No effect of agar on the functional activities of macrophages was observed. A defective intracellular killing by peritoneal macrophages due to Brewer thioglycolate was seen only after an intraperitoneal injection with thioglycolate, not after in vitro incubation of resident macrophages with thioglycolate. The results of this study show that, depending on the kind of thioglycolate used, the functional characteristics of elicited macrophages may alter. However, none of the forms of thioglycolate investigated induced the recruitment of activated macrophages.

Animals↗
PubMed2001

Toxic effects of potassium bromate and thioglycolate on vestibuloocular reflex systems of Guinea pigs and humans.

Potassium bromate (KBrO(3)) and thioglycolate are two components of hair curling solution. The neurotoxic effects of KBrO(3) and thioglycolate on the vestibuloocular reflex (VOR) system have not been elucidated. In this paper, we report the adverse effects of KBrO(3) and thioglycolate on the VOR system of Hartley-strain guinea pigs. The function of the VOR system was evaluated by caloric test coupled with the electronystagmographic recordings after subcutaneous injection of 20 or 50 mg/kg KBrO(3) or 15 mg/kg thioglycolate, either alone or in combination once daily for 14 consecutive days. The results showed that KBrO(3) produced abnormal caloric responses in a concentration-dependent manner and thioglycolate enhanced this abnormality. Our clinical patients, 10 female hairdressers exposed to the hair curling solution for 10-30 years revealed a similar dysfunction in the caloric test. The possible mechanism of this adverse effect was studied: the cerebellar-regulated functions such as motor equilibrium performance and spontaneous locomotor activity of guinea pigs were reduced, the enzymatic Na(+)/K(+)-ATPase and Ca(2+)-ATPase activities of cerebellar tissues were significantly decreased, and the loss of Purkinje cells as well as the derangement of the granular cell layer of the cerebellar cortex was revealed after treatment with KBrO(3) plus thioglycolate. These findings imply that KBrO(3) plus thioglycolate is toxic to the VOR system, mediated by, at least in part, the dysfunction of a higher cerebellar regulatory mechanism. We suggest that the caloric test is a noninvasive method for monitoring the consequences of hazardous exposure of hair curling solution in humans. Our clinical findings together with the animal study imply that clinicians should be alert to the risk of bromate exposure in hairdressers, especially those with vertigo, tinnitus, or hearing loss.

Adenosine Triphosphatases↗
PubMed1986

Kinetics of macrophage recruitment and turnover in peritoneal inflammatory exudates induced by Salmonella or thioglycollate broth.

Kinetics of peritoneal macrophage turnover during infection of mice with Salmonella enteritidis or following injection with thioglycollate broth or other peritoneal stimulants has been studied. Single intravenous injections of tritiated thymidine were given and the cells were examined by autoradiography. Maximum labelling of small adherent peritoneal macrophages occurred when 3H-thymidine was given 1 d after Salmonella and the cells were harvested 1 d later. Labelled cells decreased at later times despite maintenance of high numbers of macrophages in the exudates. Results from experiments in which labelled peritoneal cells were reinjected indicated that small, monocyte-enriched, labelled cells were not the major source of the large macrophages. Similar labelling at 2 d was observed using heat-killed Corynebacterium parvum or lipopolysaccharide (LPS) as ip stimulants. Following injection of thioglycollate broth, labelled peritoneal macrophages were only detectable if 3H-thymidine was given before the stimulant. These labelled cells remained longer in the peritoneal cavity. Labelling of and numbers of blood monocytes were consistent with the promotion of monocytopoiesis by Salmonella but not by thioglycollate. The response to thioglycollate but not Salmonella was dependent on the age of the mice. Animals injected with thioglycollate 1 d before Salmonella also had decreased resistance to bacteria and low numbers of labelled peritoneal macrophages. We propose that thioglycollate may recruit from a subset of preformed monocytes and temporarily block monocytopoiesis or macrophage bactericidal activity.

Adjuvants, Immunologic↗
PubMed1980

Thioglycolate medium decreases resistance to bacterial infection in mice.

Brewer thioglycolate medium, a bacterial culture medium which is widely used as a nonspecific in vivo macrophage stimulant, was tested for its effect on mouse resistance to bacterial infection. Mice which did or did not receive thioglycolate medium were challenged with Listeria monocytogenes. Injection of thioglycolate medium significantly decreased the ability of the host to resist infection. This decreased resistance occurred whether thioglycolate medium was injected 0 to 9 days before, or 1 to 2 h after Listeria challenge. Bacteria grew considerably better in washed adherent peritoneal cells from thioglycolate medium-injected mice than in washed adherent peritoneal cells from normal mice. Thus, thioglycolate medium may ultimately cause a decrease in macrophage function.

Animals↗
PubMed1981

Dissociation of bactericidal activity from other functions of activated macrophages in exudates induced by thioglycolate medium.

Macrophages displayed increased spreading, increased Fc-receptor-mediated phagocytosis, and increased secretion of plasminogen activator when collected from the peritoneal cavities of either Listeria-immune mice challenged intraperitoneally 3 days earlier with Listeria or nonimmune mice injected intraperitoneally 3 days earlier with fluid thioglycolate medium. In contrast, macrophages from the thioglycolate-induced peritoneal exudates were severely impaired in vitro in their ability to destroy Listeria. Injection of thioglycolate markedly interfered with the destruction of sublethal intraperitoneal challenge of Listeria, which resulted in nonimmune animals dying of an overwhelming systemic infection. In animals immune to Listeria, injection of thioglycolate delayed the onset of the expression of immunity to an intraperitoneal challenge of bacteria. The thioglycolate-induced suppression of bactericidal activity was determined to be confined to the site of injection. Results of experiments indicated that the colloidal agar in thioglycolate medium was the cause of the impairment of macrophage bactericidal activity. In addition to the impairment of bactericidal activity induced by agar, additional studies showed that an intraperitoneal injection of colloidal agar (0.075% wt/vol) by itself was a sufficient inflammatory stimulus for the accumulation of a large number of host phagocytic cells.

Agar↗
PubMed2000

The detrimental effects of potassium bromate and thioglycolate on auditory brainstem response of guinea pigs.

Potassium bromate (KBrO3) is known to be an oxidizing agent that is used not only as a food additive, mainly in the bread-making process, but also as a neutralizer in thioglycolate containing hair curling set. Although it has been shown that bromate poisoning could cause severe and irreversible sensorineural hearing loss as well as renal failure, the action mechanism of bromate-induced otoneurotoxicity especially its combination with thioglycolate remains to be studied. In this study, we attempted to investigate the toxic effects of KBrO3 in combination with or without thioglycolate on the auditory brainstem response (ABR) system in the guinea-pigs which was claimed to be very susceptible to the xenobiotics. In a preliminary test, we have found that after consecutive 2 weeks administration, KBrO3 caused a significant prolongation of wave I-III and the interwave latencies of ABR as well as significantly elevated the threshold of hearing, suggesting that the conduction velocity of the peripheral auditory nerve was delayed. By contrast, the absolute latency of wave IV/V and the interwave latency of wave III-V were not significantly prolonged, suggesting that KBrO3 had no effect on the brainstem. This oto-neurotoxic effect of KBrO3 was markedly enhanced by combining with thioglycolate. Our data also indicated that KBrO3 combined with thioglycolate but not KBrO3 alone prominantly caused a decrease of body weight. However, enzymatic activities (including Na+/K+-ATPase and Ca2+-ATPase) and the level of nitric oxide (NO) was significantly affected in the brainstem. Based on these findings, we tentatively conclude that whether KBrO3 alone or KBrO3 combined with thioglycolate induced oto-neurotoxicity majorly through the peripheral auditory nerve rather than via the central brainstem intoxication.

Animals↗
PubMed1981

The oxidative metabolism of thioglycollate-elicited mouse peritoneal macrophages: the relationship between oxygen, superoxide and hydrogen peroxide and the effect of monolayer formation.

The oxygen and glucose metabolism of peritoneal macrophages harvested from untreated mice (resident cells) and mice given an i.p. injection of thioglycollate broth (thioglycollate cells) were examined. Thioglycollate cells consumed approximately 3 times as much O2 at rest and during phagocytosis as resident cells, but oxygen reduction products (superoxide and hydrogen peroxide) could be recovered in only minimal amounts despite triggering by phagocytosis or exposure to PMA. Indirect evidence for the formation of oxygen reduction products such as O2- by thioglycollate cells was obtained by observation of the major pathways for glucose oxidation and NBT dye reduction. When thioglycollate cells were allowed to adhere to a glass surface O2- and H2O2 were easily recovered in the extracellular medium with a 20-fold increase above cells in suspension exposed to PMA. This study suggests that thioglycollate-elicited macrophages have a vigorous oxidative metabolism but that recovery, and perhaps utilization, of O2 reduction products formed will depend on the conditions of incubation. These events may be significant both for the study of parameters of macrophage "activation" in vitro as well as the function of these cells in vivo.

Animals↗
PubMed1995

Increased phospholipid mass with decreased arachidonoyl molecular species is associated with decreased eicosanoid synthesis and increased tumor necrosis factor synthesis by thioglycollate-elicited rat peritoneal macrophages.

Because the activation state of macrophages may alter their response to endotoxin, we compared phospholipid arachidonic acid content, and synthesis of eicosanoids and tumor necrosis factor by resident and thioglycollate-elicited rat peritoneal macrophages. Thioglycollate elicitation increased macrophage phospholipid mass twofold, increased the relative percentages of 16:0-20:4 diacylglycerophosphocholine (PtdCho) and 18:0-20:4 diacylglycerophosphoethanolamine (PtdEtn), and decreased the relative percentages of 18:0-20:4 alkenylacylglycerophosphoethanolamine (PlsEtn) and 18:0-20:4 alkylacylglycerophosphocholine (PakCho) compared with resident peritoneal macrophages. Thioglycollate-elicited macrophages synthesized significantly less thromboxane B2, 6-keto-prostaglandin F1 alpha, and prostaglandin E2 and more tumor necrosis factor (TNF) activity in response to both endotoxin and A23187 than did resident macrophages. These results suggest that thioglycollate elicitation decreases specific arachidonic acid-containing molecular species in PlsEtn and PakCho, which may, in part, explain the decrease in eicosanoid and increase in TNF synthesis by thioglycollate-elicited macrophages. The differences between resident and thioglycollate-elicited macrophages in the synthesis of the eicosanoids and TNF activity was not altered by increasing either the concentration of either stimulus or the incubation time.

Animals↗
PubMed1994

Regulation of lipopolysaccharide-induced tumor necrosis factor alpha production by endogenous prostaglandin E2 in rat resident and thioglycollate-elicited macrophages.

Prostaglandin E2 (PGE2) is generally accepted to be a negative feedback effector of tumor necrosis factor alpha (TNF alpha) production. However, we have observed that a cyclooxygenase inhibitor had different effects on TNF alpha production by resident and thioglycollate-elicited rat peritoneal macrophages. Indomethacin coordinately reduced PGE2 production and increased TNF alpha production in lipopolysaccharide (LPS)-stimulated resident macrophages, whereas indomethacin reduced PGE2 production without affecting TNF alpha production in thioglycollate-elicited macrophages. PGE2 production and arachidonate release were much less in thioglycollate-elicited macrophages than in resident macrophages. However, exogenously added PGE2 suppressed TNF alpha production to the same extent in the two macrophage populations. The addition of free arachidonic acid to cultures of LPS-stimulated, thioglycollate-elicited macrophages elevated PGE2 production and suppressed TNF alpha production in a manner similar to that observed with LPS-stimulated resident macrophages. These results indicate that the differential effects of indomethacin treatment on TNF alpha production observed between the two macrophage populations are not due to the differences in arachidonate contents, PGE2 productivities, nor to their capacities to respond to PGE2. Instead, the inability of indomethacin to increase TNF alpha production by thioglycollate-elicited versus resident macrophages appears to result from an inability to release arachidonate efficiently and a lower initial level of cyclooxygenase, in thioglycollate-elicited macrophages.

Animals↗
PubMed1989

The use of thioglycolate to distinguish between 3' AP (apurinic/apyrimidinic) endonucleases and AP lyases.

Addition of thioglycolate and DEAE-Sephadex chromatography were used to analyze the cleavage of the C(3')-O-P bond 3' to AP (apurinic/apyrimidinic) sites in DNA and to distinguish between a mechanism of hydrolysis (which would allow the nicking enzyme to be called 3' AP endonuclease) or beta-elimination (so that the nicking enzyme should be called AP lyase). For this purpose, DNA labelled in the AP sites was first cleaved by rat-liver AP endonuclease, then with the 3' nicking catalyst in the presence of thioglycolate and the reaction products were analyzed on DEAE-Sephadex: deoxyribose-5-phosphate (indicating a 3' cleavage by hydrolysis) and the thioglycolate:unsaturated sugar-5-phosphate adduct (indicating a cleavage by beta-elimination) are well separated allowing to eventually easily discard the hypothesis of a hydrolytic process and the appellation of 3' AP endonuclease. We have shown that addition of thioglycolate to the unsaturated sugar resulting from nicking the C(3')-O-P bond 3' to AP sites by beta-elimination is an irreversible reaction. We have also shown that the thioglycolate must be present from the beginning of the reaction with the nicking catalyst to prevent the primary 5' product of the beta-elimination reaction from undergoing other modifications that complicate the interpretation of the results.

Animals↗
PubMed2002

Effect of enriched thioglycolate on direct examination of respiratory specimens and guiding initial empirical therapy in intubated patients with pneumonia: a prospective, randomized study.

OBJECTIVE: To evaluate the use of enriched thioglycolate as a transport medium of protected specimen brush samples, in particular its value in direct examination of respiratory specimens and in guiding initial antibiotic prescription. DESIGN: Prospective, randomized, pilot study. SETTING: Medical-surgical teaching intensive care unit. SUBJECTS: Thirty adults with suspected ventilator-associated pneumonia. INTERVENTION: Bronchoscopy was performed by using standard techniques, and two consecutive protected specimen brush samples were taken. Transport medium consisted of 1 mL of sterile saline or thioglycolate. Gram stains were performed in all samples. Randomization was used to select which transport medium was used first. Each patient served as his or her own control. The laboratory was blind to the choice. MEASUREMENTS AND MAIN RESULTS: Causative agents were cultured in 16 episodes, and no significant differences were observed when the transport media were compared. Anaerobes were identified in only one episode. Direct staining in thioglycolate samples anticipated the presumptive diagnosis (in presence of false-negative cultures) in three additional patients in whom prior antibiotic therapy was prescribed; this was also the case in one patient with saline solution. The etiology was anticipated by direct Gram staining and permitted a more targeted initial empirical treatment in 75% of samples transported in thioglycolate, compared with only 37.5% of samples transported in saline solution (p <.05). CONCLUSION: When protected specimen brush samples are obtained, thioglycolate may contribute to early identification of the pathogen and may guide the initial empirical therapy.

Adult↗
PubMed1987

Thioglycollate elicited macrophages demonstrate enhanced virus replication and depressed bacterial killing.

Thioglycollate elicited peritoneal macrophages of Balb/c mice exhibited minimal antibacterial activity against Listeria monocytogenes but were fully permissive for the replication of ectromelia virus. By comparison, resident and LPS elicited macrophages did not exhibited depressed antibacterial activity nor did they support viral replication. The thioglycollate effects were demonstrated in macrophages cultured in vitro and also in intact Balb/c mice. Mice given thioglycollate intraperitoneally and challenged by the same route suffered overwhelming virus and bacterial infections as a result of early local proliferation within peritoneal macrophages with subsequent spread to the liver. Balb/c mice challenged intravenously with similar doses of the virus of bacterial pathogen after administration of thioglycollate by the i.p. route did not succumb to either infection. Thus the ability of thioglycollate to compromise cellular host defenses against the infectious agents appears to be site specific; i.e. restricted to the peritoneal cavity where exudate macrophages and challenge inocula first come into contact.

Animals↗
PubMed2003

Developmental toxicity evaluation of sodium thioglycolate administered topically to Sprague-Dawley (CD) rats and New Zealand White rabbits.

BACKGROUND: Sodium thioglycolate, which has widespread occupational and consumer exposure to women from cosmetics and hair-care products, was evaluated for developmental toxicity by topical exposure during the embryonic and fetal periods of pregnancy METHODS: Timed-mated Sprague-Dawley rats (25/group) and New Zealand White (NZW) rabbits (24/group) were exposed to sodium thioglycolate in vehicle (95% ethanol:distilled water, 1:1) by unoccluded topical application on gestational days (GD) 6-19 (rats) or 6-29 (rabbits) for 6 hr/day, at 0, 50, 100, or 200 mg/kg body weight/day (rats) and 0, 10, 15, 25, or 65 mg/kg/day (rabbits). At termination (GD 20 rats; GD 30 rabbits), fetuses were examined for external, visceral, and skeletal malformations and variations. RESULTS: In rats, maternal topical exposure to sodium thioglycolate, at 200 mg/kg/day (the highest dose tested) on GD 6-19, resulted in maternal toxicity, including reduced body weights and weight gain, increased relative water consumption and one death. Treatment-related increases in feed consumption and changes at the applicationsite occurred at all doses, in the absence of increased body weights or body weight change. Fetal body weights/litter were decreased at 200 mg/kg/day, with no other embryo/fetal toxicity and no treatment-related teratogenicity in any group. In rabbits, maternal topical exposure to sodium thioglycolate on GD 6-29 resulted in maternal dose-related toxicity at the dosing site in all groups; no maternal systemic toxicity, embryo/fetal toxicity, or treatment-related teratogenicity were observed in any group. CONCLUSIONS: A no observed adverse effect level (NOAEL) was not identified for maternal toxicity in either species with the dosages tested. The developmental toxicity NOAEL was 100 mg/kg/day (rats) and > or = 65 mg/kg/day (rabbits; the highest dose tested). The clinical relevance of theses study results is uncertain because no data were available for levels, frequency, or duration of exposures in female workers or end users.

Abnormalities, Drug-Induced↗
PubMed1989

The effect of thioglycolate on intermediate filaments and membrane translocation in rat urothelium during the expansion-contraction cycle.

The functional role of cytokeratin intermediate filaments in the translocation of asymmetric membrane plaques between cytoplasm and surface of apical urothelial cells was investigated during contraction and expansion of rat urinary bladders. A stereological investigation of electron micrographs provided estimations of surface area, volume, and number of discoidal vesicles and infoldings per unit volume of urothelial apical cell cytoplasm. Contracted and distended bladders incubated in 0.01 M sodium bicarbonate were compared to identical preparations experimentally incubated in 5 mM thioglycolic acid. The latter reagent disrupts the intermediate filament network by reducing sulfhydryl bridges. Densities of discoidal vesicles in cells contracted after incubation in thioglycolate were similar to density estimations in cells expanded under control conditions. Similarly, densities of vesicles in cells expanded after exposure to thioglycolate were comparable in number to those in normally contracted cells. Thus, membrane translocation to and from the luminal surface was blocked by thioglycolate treatment. The lack of normal membrane transfer at the luminal surface induces apical cells exposed to experimental conditions to undergo extraordinary adjustments in response to external pressures of bladder contraction and distension. During contraction, the apical-intermediate cell interface unfolded while the luminal surface ballooned out into the lumen. In distended bladders, large intercellular spaces formed between apical cells along their lateral margins. The results support a model published earlier implicating the filament network as a critical mediator of membrane translocation.

Animals↗