Effect of whole body cryotherapy on low back pain and release of endorphins and stress hormones in patients with lumbar spine osteoarthritis.

Introduction: Low back pain (LBP) is the most common ailment in patients with lumbar spine osteoarthritis (OA). There are many methods to treat LBP, such as manual therapy, osteopathy, massage, physical exercise, and physical therapy. The most effective of these are manual therapy and exercises combined with physical procedures, such as whole body cryotherapy (WBCT). Whole body cryotherapy can induce various hormonal adaptations in patients with OA. This is probably the body's reaction to cold and stress. The purpose of the study was to evaluate the impact of WBCT on ß-endorphins, cortisol and adrenaline release, as well as on LBP in patients with OA of the lumbar spine. Material and methods: The study group consisted of 30 patients with lumbar spine OA who underwent a series of WBCT combined with therapeutic exercises. Before and after the therapy each patient was examined using a visual analogue scale (VAS) and blood samples were collected for laboratory determinations (ELISA). Results: After WBCT, the decrease in LBP measured by VAS was statistically significant (p < 0.0001). The mean value of blood ß-endorphin level increased after the therapy but the difference was statistically insignificant (p = 0.10). The mean value of the plasma level of cortisol after treatment increased and the difference was statistically significant (p = 0.0009). The plasma level of adrenalin after treatment increased slightly, but the difference was statistically insignificant (p = 0.08). Conclusions: Whole body cryotherapy combined with therapeutic exercises had a positive effect on LBP reduction in patients with OA. On the basis of these changes, processes that take place in the nervous and endocrine systems are a response to the stimuli of cold and stress. The mechanism of action of extremely low temperatures on the human body is still not fully understood.

Chemerin alleviates acute pancreatitis in the rat thorough modulation of NF-κB signal.

OBJECTIVE: Chemerin, an adipokine, works as the chemoattractant for the immune cells. The role of chemerin in the inflammatory reaction is controversial. Chemerin has been shown to aggravate the inflammatory response, but other studies demonstrated its anti-inflammatory influence. This study assessed the effects of chemerin on acute pancreatitis (AP) in vivo and in vitro. METHODS: For in vivo experiments male Wistar rats were used. For in vitro study rat pancreatic AR42J cells were employed. Chemerin (1, 5 or 10 µg/kg) was given to the rats prior to the induction of AP by subcutaneous caerulein infusion (25 µg/kg). For in vitro studies cells were subjected to caerulein (10 nM) with or without chemerin (100 nM). Serum amylase activity was measured by enzymatic method, serum TNFα concentration - by ELISA kit. Western-blot was used to examine cellular proteins. RESULTS: AP was confirmed by histological examination. Chemerin given to AP rats decreased histological manifestations of AP, reduced serum amylase activity and TNFα concentration. In AR42J cells subjected to caerulein with addition of chemerin signal for TNFα was reduced comparing to the cultures treated with caerulein alone. Analysis of the dynamics of nuclear translocation for p50, p65 and Bcl-3 points out to NF-κB attenuation as a mechanism of observed anti-inflammatory action of chemerin. CONCLUSION: Chemerin significantly alleviated severity of AP in the rat, this is possibly due to the inhibition of pro-inflammatory signaling in the pancreatic cells.

Effects of Melatonin and Its Analogues on Pancreatic Inflammation, Enzyme Secretion, and Tumorigenesis.

Melatonin is an indoleamine produced from the amino acid l-tryptophan, whereas metabolites of melatonin are known as kynuramines. One of the best-known kynuramines is N¹-acetyl-N¹-formyl-5-methoxykynuramine (AFMK). Melatonin has attracted scientific attention as a potent antioxidant and protector of tissue against oxidative stress. l-Tryptophan and kynuramines share common beneficial features with melatonin. Melatonin was originally discovered as a pineal product, has been detected in the gastrointestinal tract, and its receptors have been identified in the pancreas. The role of melatonin in the pancreatic gland is not explained, however several arguments support the opinion that melatonin is probably implicated in the physiology and pathophysiology of the pancreas. (1) Melatonin stimulates pancreatic enzyme secretion through the activation of entero-pancreatic reflex and cholecystokinin (CCK) release. l-Tryptophan and AFMK are less effective than melatonin in the stimulation of pancreatic exocrine function; (2) Melatonin is a successful pancreatic protector, which prevents the pancreas from developing of acute pancreatitis and reduces pancreatic damage. This effect is related to its direct and indirect antioxidant action, to the strengthening of immune defense, and to the modulation of apoptosis. Like melatonin, its precursor and AFMK are able to mimic its protective effect, and it is commonly accepted that all these substances create an antioxidant cascade to intensify the pancreatic protection and acinar cells viability; (3) In pancreatic cancer cells, melatonin and AFMK activated a signal transduction pathway for apoptosis and stimulated heat shock proteins. The role of melatonin and AFMK in pancreatic tumorigenesis remains to be elucidated.

[Immunological mechanisms involved in obesity and their role in metabolic syndrome]. / Mechanizmy immunologiczne towarzyszace otylosci i ich rola w zaburzeniach metabolizmu.

In the past 50 years, the occurrence of human obesity has risen dramatically across the globe. The WHO reported that at least 1.9 billion (1.9 × 10(9)) adults are overweight and 600 million are obese, and the numbers are expected to rise dramatically in the future without intervention. The recent increase in human obesity is caused by increased energy intake and reduced energy expenditure that results in a massive increase in adipose tissue, which is generally harmful to our health. Indeed, the increase in human obesity is strongly associated with an increase in many diseases such as type 2 diabetes (T2D), biliary disease, cardiovascular disease, hepatic steatosis, airway disease, neurodegeneration and certain cancers. The metabolic and immune systems are closely linked and functionally dependent. As a result, excessive nutrient consumption associated with obesity can be recognized as a harmful, stress-inducing biological event by innate pattern recognition receptors (PRRs). This activates inflammatory and stress responses in various metabolic tissues, leading to the chronic low-grade inflammation called metabolic inflammation or "metainflammation". Adipose tissue is mainly composed of adipocytes, although other cell types contribute to its growth and function, including pre-adipocytes, macrophages, lymphocytes, fibroblasts and vascular cells. Obesity can result in profound changes in the cell composition of fat tissue and can lead to the modulation of individual cell phenotypes. Many factors are involved in development of metainflammation, including hypoxia of adipocytes, oxidative stress, endoplasmic reticulum stress, activation of inflammasomes, adipocyte death, activation of TLR and abnormal gut flora.

Paracetamol (acetaminophen) decreases hydrogen sulfide tissue concentration in brain but increases it in the heart, liver and kidney in mice.

The biological action ofN-acetyl-p-aminophenol - paracetamol (acetaminophen) has been demonstrated to involve different mechanisms and is still not clear. Hydrogen sulfide (H2S) has been shown to play an important role in many physiological and pathological processes including nociception. The interaction between acetaminophen and endogenous H2S is unknown. Twenty four female CBA strain mice were administered intraperitoneal injections of N-acetyl-p-aminophenol solution: paracetemol in doses of 30 mg/kg b.w. per day (group D1, n = 8) or 100 mg/kg b.w. per day (group D2, n = 8).. The control group (n = 8) received physiological saline in portions of the same volume--0.2 ml. The measurements of tissue H2S concentration were performed with the Siegel spectrophotometric modified method. In the brain, the H2S tissue level decreased, but more significantly in the lower drug dose group. Conversely, there was a significant rise in the H2S tissue concentration in D1 and D2 groups in heart and kidney with the increase more pronounced in the group with the lower paracetamol dose. In the liver only the higher acetaminophen dose elicited a change in H2S concentration, increasing after administration of acetaminophen at 100 mg/kg. Our study demonstrates that paracetamol induces H2S tissue concentration changes in different mouse organs.

Carvedilol induces endogenous hydrogen sulfide tissue concentration changes in various mouse organs.

Carvedilol, a third generation non-selective adrenoreceptor blocker, is widely used in cardiology. Its action has been proven to reach beyond adrenergic antagonism and involves multiple biological mechanisms. The interaction between carvedilol and endogenous 'gasotransmitter' hydrogen sulfide (H2S) is unknown. The aim of the study is to assess the influence of carvedilol on the H2S tissue level in mouse brain, liver, heart and kidney. Twenty eight SJL strain female mice were administered intraperitoneal injections of 2.5 mg/kg b.w./d (group D1, n=7), 5 mg/kg b.w./d (group D2, n=7) or 10 mg/kg b.w./d of carvedilol (group D3, n=7). The control group (n=7) received physiological saline in portions of the same volume (0.2 ml). Measurements of the free tissue H2S concentrations were performed according to the modified method of Siegel. A progressive decline in H2S tissue concentration along with an increase in carvedilol dose was observed in the brain (12.5%, 13.7% and 19.6%, respectively). Only the highest carvedilol dose induced a change in H2S tissue level in the heart - an increase by 75.5%. In the liver medium and high doses of carvedilol increased the H2S level by 48.1% and 11.8%, respectively. In the kidney, group D2 showed a significant decrease of H2S tissue level (22.5%), while in the D3 group the H2S concentration increased by 12.9%. Our study has proven that carvedilol affects H2S tissue concentration in different mouse organs.

Amlodipine affects endogenous hydrogen sulfide tissue concentrations in different mouse organs.

The interactions between calcium channel blockers' action and the endogenous hydrogen sulfide (H2S) biology are unknown. CBA strain mice were administered intraperitoneally 3 mg/kg b.w. per day or 10 mg/kg b.w. per day of amlodipine. The control group received physiological saline. The measurements of the free H2S tissue concentrations were performed with Siegel spectrophotometric modified method. There was as significant fall of H2S level in the brain and the liver in both groups. The lower amlodipine dose increased the H2S concentrations in the heart and kidneys while the higher one decreased H2S accumulation in those organs. Our experiment has shown that amlodipine interferes with H2S biology and affects its tissue concentrations in different mouse tissues.

Ramipril affects hydrogen sulfide generation in mouse liver and kidney.

Hydrogen sulfide (H2S) is a modulator of various physiological and pathological processes in the cardiovascular and nervous system and plays an important role in the regulation of gastrointestinal tract, liver and kidney function. The effect of the pleiotropic action of the tissue specific angiotensin-converting enzyme inhibitor (ACEI), ramipril, exceeds renin-angiotensin aldosterone system (RAAS) blockade and involves different biological mechanisms. The aim of the study is to assess the influence of ramipril on H2S production in mouse liver and kidneys. Thirty mice (CBA) of both sexes were given intraperitoneal injections of ramipril solutions--0.125 mg (5 mg/kg--group D1) and 0.25 mg (10 mg/kg--group D2) for 5 consecutive days at the same time of the day (10:30 am). The control group received physiological saline in portions of the same volume--0.2 ml. The measurements of the tissue concentration of H2S were performed using the modified spectrophotometric method of Siegel. There was a significant rise in the tissue concentration of H2S [microg/g] in livers of group D1 (2.70 +/- 0.02 vs 2.81 +/- 0.06; P = 0.03) and group D2 (2.70 +/- 0.02 vs 2.98 +/- 0.03; P < 0.001) and a significant decrease of H2S kidney tissue concentration in group D1 (3.35 +/- 0.06 vs 3.15 +/- 0.07; P = 0.02) and in group D2 (3.35 +/- 0.06 vs 2.89 +/- 0.03; P < 0.001). Our results show that ACEI ramipril affects hydrogen sulfide generation in mouse liver and kidneys.

The Opposite Effect of L-kynurenine and Ahr Inhibitor Ch223191 on Apoptotic Protein Expression in Pancreatic Carcinoma Cells (Panc-1).

BACKGROUND: L-kynurenine, derivate of L-tryptophan, is synthetized by indoleamine 2,3-dioxygenase (IDO). The effects of L-kynurenine depend on its binding to an aryl hydrocarbon receptor (AhR). OBJECTIVE: The aim of this study was to investigate the changes within the apoptotic pathway in PANC-1 cells subjected to L-kynurenine or L-tryptophan considering the production of anti-apoptotic proteins from the IAPs and Bcl-2 family, as well as the regulation of NF-κB signaling. METHODS: The investigated substances were added alone or in combination with the AhR inhibitor (CH223191) to cultures of PANC-1 cells. Cytoplasmic and nuclear proteins were analyzed by immunoblotting and cells were incubated with the investigated substances to determine cytotoxicity and proliferative effects. RESULTS: Incubation of PANC-1 cells with L-kynurenine or L-tryptophan resulted in the increase in antiapoptotic cIAP-1, cIAP-2, XIAP and Bcl-2 expression and a decrease in pro-apoptotic Bax. These changes were accompanied by the reduction of active caspases -9, -3 and PARP-1. The treatment leads to translocation and enhanced production of nuclear NF-κB p50 and Bcl-3. Incubation of the cells with AhR blocker either alone or together with L-kynurenine or L-tryptophan resulted in the opposite effect, leading to the downregulation of IAPs and Bcl-2, upregulation of Bax and caspases expression. CONCLUSION: 1) L-kynurenine and its precursor promote anti-apoptotic effects through the modulation of IDOdependent pathway and regulation of IAPs, Bcl-2 and NF-κB family members in pancreatic carcinoma cells 2) inhibition of AhR by CH223191 exerts an apoptosis-promoting effect, and this observation might suggest the potential use of this compound in pancreatic cancer therapy.

The effect of aspirin on Gomori-positive glia in mouse brain.

Aspirin (acetylsalicylic acid, ASA) treatment resulted in a significant decrease in the amount of the sulfur-rich Gomori-positive material present in the cytoplasm of periventricular glia. It also caused the accumulation of the Gomori-positive neurosecretory material in the supraoptic and paraventricular nuclei and, most pronounced, in the neurosecretory axons of the paraventricular- and supraoptic-neurophypophysial tract.

Ramipril enhances the endogenous hydrogen sulfide tissue concentration in mouse heart and brain.

BACKGROUND: Hydrogen sulfide (H2S) participates in regulation of different physiological and pathological processes of cardiovascular system and nervous system. The effect of ramipril - tissue specific angiotensin-converting enzyme inhibitor (ACEI) - exceeds renin-angiotensin aldosterone system (RAAS) blockade. The influence of ACEI on the metabolism of H2S remains obscure. The aim of the study is to assess the impact of ramipril administration on the tissue concentration of H2S in mouse heart and brain. METHOD: Thirty mice (CBA) of both sexes were given intraperitoneal injections of ramipril solution - 0.125 mg (5 mg/kg - group D1) and 0.25 mg (10 mg/kg - group D2) for 5 consecutive days at the same time of the day (10:30 am). Control group received physiological saline in portions of the same volume - 0.2 ml. The measurements of the concentration of H2S were performed using spectrophotometric modified method of Siegel. RESULTS: There has been a significance rise in the tissue concentration of H2S [microg/g] in the heart in group D1 (4.91 +/- 0.07 vs 5.54 +/- 0.12; p = 0.005) and group D2 (4.91 +/- 0.07 vs 5.94 +/- 0.08; p < 0.001) and in the brain in group D1 (0.61 +/- 0.03 vs 0.69 +/- 0.02; p = 0.02) and non-significant increase in the brain D2 group (0.61 +/- 0.03 vs 0.65 +/- 0.03; p = 0.16). CONCLUSIONS: Ramipril enhances the concentration of endogenous H2S in mouse heart and brain.

Melatonin and its metabolite N1-acetyl-N2-formyl-5-methoxykynuramine (afmk) enhance chemosensitivity to gemcitabine in pancreatic carcinoma cells (PANC-1).

BACKGROUND: Gemcitabine is a standard chemotherapeutic agent for patients suffering from pancreatic cancer. However, the applied therapy is not effective due to the resistance of tumor cells to cytostatics, caused by inefficiency of the apoptotic mechanisms. Herein, we present the hypothesis that melatonin and its metabolite N1-acetyl-N2-formyl-5-methoxykynuramine (AFMK) modify the effect of gemcitabine on PANC-1 cells and that this phenomenon is dependent on the modulation of apoptosis. METHODS: PANC-1 cells have been incubated with melatonin, AFMK or gemcitabine alone or in combination to determine the cytotoxity and proliferative effects. In subsequent part of the study, cells were harvested, the proteins were isolated and analyzed employing immunoprecipitation/immunoblotting. RESULTS: Incubation of PANC-1 cells with gemcitabine resulted in upregulation of pro-apoptotic bax and caspases proteins expression, downregulation of anti-apoptotic Bcl-2, heat shock proteins (HSPs) and modulation of cellular inhibitors of apoptosis (IAPs). Both melatonin and AFMK administered to PANC-1 in combination with gemcitabine inhibited the production of HSP70 and cIAP-2 as compared to the results obtained with gemcitabine alone. These changes were accompanied by upregulation of Bax/Bcl-2 ratio and reduction of procaspases-9 and -3 abundance, followed by an increase in the formation of active caspase of PANC-1 cells with combination of gemcitabine plus low doses of melatonin or AFMK led to enhanced cytotoxicity and resulted in the inhibition of PANC-1 cells growth as compared to effects of gemcitabine alone. CONCLUSION: Melatonin and AFMK could improve the anti-tumor effect of gemcitabine in PANC-1 cells presumably through the modulation of apoptotic pathway.

Aspirin augments the concentration of endogenous hydrogen sulfide in mouse brain and liver.

Intraperitoneal injections of lysine acetylsalicylate (L-ASA, aspirin) in a dose of 10 mg during 5 consecutive days to BALB/c and B10.PL mice increased the concentration of endogenous hydrogen sulfide in their livers. The rise of hydrogen sulfur levels was shown also in brains of BALB/c females and B10.PL males, however in BALB/c male brains there is no statistically significant difference. The mechanism of aspirin action on H2S concentration is discussed.

Effects of acetylsalicylic acid on the levels of sulfane sulfur and non-protein sulfhydryl groups in mouse tissues.

BACKGROUND: The study is focused on searching for the link between acetylsalicylic acid (ASA) and sulfur metabolism. The present work aimed to investigate the effect of ASA on the level of the sulfane sulfur and non-protein thiol compounds (NPSH) in the liver and kidneys of mice. METHODS: The study was conducted on female albino Swiss mice weighing approximately 20 g. The experimental group was treated intraperitoneally (ip) with aspirin, lysine salt, at a dose of 10 mg (on pure aspirin basis)/kg for 5 days. The control group was treated ip with 0.9% NaCl in a volume of 0.2 ml for 5 days. The experimental and control mice were sacrificed by cervical dislocation on 5th day of the experiment, 3 h after the last injection. The homogenates of livers and kidneys were next used for assaying the levels of NPSH and sulfane sulfur-containing compounds. RESULTS: The results indicate that in the liver of ASA-treated mice, the level of the cyanolysable sulfane sulfur decreased compared to the control group, whereas in the kidney, its level significantly increased. The opposite results in the liver and kidney were observed also for NPSH, namely ASA elicited a drop in NPSH level in the liver, and elevated it in the kidney. CONCLUSION: The results of the present study suggest that ASA affects sulfur metabolism, in particular, renal and hepatic production of sulfane sulfur and NPSH in mice.

Epicutaneous immunization with protein antigen TNP-Ig alleviates TNBS-induced colitis in mice.

BACKGROUND: Ulcerative colitis (UC) is a chronic inflammatory autoimmune disease with limited treatment modalities. The animal model of colitis induced by treatment with trinitrobenzene sulfonic acid (TNBS-colitis) is commonly used to test new therapies of this disease. In our previous work we found that epicutaneous (EC) immunization with protein antigen induced a state of profound immunosuppression that inhibited inflammatory response in contact sensitivity, in experimental autoimmune encephalomyelitis (EAE) and in allogeneic skin graft rejection. METHODS: TNBS-induced colitis was used as an experimental model. RESULTS: In our current work, we showed that EC immunization with TNP-conjugated mouse immunoglobulin (TNP-Ig) prior to induction of TNBS-colitis alleviates disease severity what was determined by the body weight, the length and the weight of the colon, the histological activity index (HAI) and myeloperoxidase activity (MPO). Observed amelioration of the disease in TNP-Ig patched mice was accompanied with decreased production of IFN-γ and IL-17A by splenocytes. Additionally, spleen cells isolated from mice EC immunized with TNP-Ig prior to colitis induction showed increased production of IL-10 suggesting that this cytokine might be involved in inhibiting inflammatory response in the colon. CONCLUSION: This work shows that EC immunization with protein antigen prior to TNBS-colitis induction ameliorates disease and observed suppression of inflammatory response in the colon might be mediated by IL-10.

Digoxin increases hydrogen sulfide concentrations in brain, heart and kidney tissues in mice.

The interest in digoxin has recently increased due to the expanding knowledge regarding endogenous cardiac glycosides and a potential oncological application of this drug. Hydrogen sulfide (H(2)S), a crucial co-modulator of various physiological processes, is involved in the pathophysiology of different disorders and may be useful in the treatment of some diseases. The interaction between cardiac glycosides and H(2)S is unknown. The aim of the study is to assess the influence of digoxin on H(2)S tissue concentrations in mouse brain, heart and kidney. Thirty male BALB/c mice were given intraperitoneal injections of digoxin at 0.5 mg/kg body weight (b.w.) per day (group D1, n = 10) or 1 mg/kg b.w. per day (group D2, n = 10). The control group (n = 10) received physiological saline. Free H(2)S tissue concentrations were measured via the Siegel spectrophotometric modified method. There was a significant, progressive increase in the H(2)S concentrations for both the low and high digoxin doses in the brain (7.7% and 8.5%, respectively), heart (by 6.0% and 22.1%, respectively) and kidney (by 7.6% and 13.0%, respectively). This report shows that digoxin administration is followed by an increase in the free H(2)S concentrations in mouse brain, heart and kidney tissues.

Atorvastatin affects the tissue concentration of hydrogen sulfide in mouse kidneys and other organs.

Hydrogen sulfide (H2S) is a crucial co-modulator of cardiovascular, nervous, digestive and excretory systems function. The pleiotropic action of atorvastatin exceeds simple 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibition and involves multiple biological mechanisms. This study assesses the influence of atorvastatin on the H2S tissue concentration in mouse brain, liver, heart and kidney. Twenty-four female CBA strain mice received an intraperitoneal injection. The mice were given one of the following solutions: 0.1 mg atorvastatin (5 mg/kg of body weight (b.w.)/day--group D1, n=8), 0.4 mg atorvastatin (20 mg/kg b.w./day--group D2, n=8) or a saline physiological control (0.2 ml--group C, n=8). A modified Siegel spectrophotometric method was used for the H2S tissue concentration measurements. There was a remarkable rise in the H2S concentration [µg/g] in the kidney (C: 5.26±0.09, D1: 5.77±0.11, p=0.0003; D2: 7.48±0.09, p<0.0001). There were also slight H2S tissue level changes in the brain (C: 1.61±0.01, D1: 1.75±0.03, p=0.0001; D2: 1.78±0.03, p<0.0001), the heart (C: 4.54±0.08, D1: 4.86±0.10, p=0.0027; D2: 4.56±0.07, p=0.6997) and the liver (C: 3.45±0.03, D1: 3.27±0.02, p=0.0001; D2: 3.31±0.02, p=0.0003). Our study supports the influence of atorvastatin on H2S tissue concentration in kidneys and other mouse organs.

Effects of aspirin on the levels of hydrogen sulfide and sulfane sulfur in mouse tissues.

This study was designed to investigate the effect of aspirin (ASA) on anaerobic cysteine metabolism, which yields sulfane sulfur-containing compounds and hydrogen sulfide (H(2)S), in mouse liver and brain. In order to solve this problem, we determined the levels of sulfane sulfur and H(2)S, and the activities of cystathionase, the enzyme directly engaged in H(2)S synthesis, and rhodanese, the enzyme that catalyzes sulfane sulfur transfer to different acceptors. Moreover, we examined the effect of ASA on glial Gomori-positive cells (GGPC) in the brain that contain sulfur-rich glial Gomori-positive material (GGPM). The studies indicated an ASA-induced decrease in H(2)S levels in the brain and an increase in the liver. ASA-treated animals had lower cerebral levels of GGPM-containing GGPCs but the sulfane sulfur level was not affected. Conversely, the sulfane sulfur content in the liver dropped. ASA did not change cystathionase and rhodanese activity in either organ. The obtained results revealed that ASA was able to influence anaerobic cysteine metabolism, leading to the formation of sulfane sulfur and H(2)S in the mouse liver and brain, and to affect the numbers of GGPM-containing GGPCs.

The glial Gomori-positive material is sulfane sulpfur.

The Gomori-positive glia are periventricular astrocytes with abundant cytoplasmic granular material, predominantly occupying a periventricular site in the brain. These granular inclusions are strongly stained with chrome hematoxylin in the Gomori's method as well as exhibit red autofluorescence and non-enzymatic peroxidase activity. The glial Gomori-positive material (GGPM) granules are positive in the performic acid Alcian blue method indicating the presence of protein-bound sulfur, what has been shown by our previous studies. The number of cells containing glial Gomori-positive granules dropped after administration of cyanide and increased under the influence of sulfane sulfur donor (diallyl disulfide). This suggests, that sulfur of these granules is a sulfane sulfur, possibly in the form of protein-bound cysteine persulfide. Sulfane sulfur is labile, reactive sulfur atom covalently bound to another sulfur atom. In this paper we present evidence that GGPM exhibit affinity to cyanolysis and its stainability in Gomori's method is due to the presence of protein-bound sulfane sulfur. The biological role of the Gomori-positive glia connected with protective properties of sulfane sulfur has been discussed.