ONION TOPICAL
- Thread starter Dashtoronto
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..... with a bag on my head ¬_¬ rofl
G
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viper3two said:
:agree:
squeegee
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Hydrogen sulfide is an endogenous stimulator
of angiogenesis
http://www.pnas.org/content/early/2009/12/01/0908047106.full.pdf
[h=1]Hydrogen sulfide, the next potent preventive and therapeutic agent in aging and age-associated diseases.[/h]
http://www.ncbi.nlm.nih.gov/pubmed/23297346
of angiogenesis
http://www.pnas.org/content/early/2009/12/01/0908047106.full.pdf
[h=1]Hydrogen sulfide, the next potent preventive and therapeutic agent in aging and age-associated diseases.[/h]
http://www.ncbi.nlm.nih.gov/pubmed/23297346
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good points
squeegee
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saintsfan92344
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I have been doing some research into this as well, I am having a period of massive hair loss so you can imagine how I am looking at anything and everything, I used it twice in the evening before showering, left it in for about 45 min or so, no irritation, but I can still smell it after showering in the morning also. I really don't do well on the meds so I am looking at the alternative options which I realize is probably useless, but got to do something
squeegee
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Jacob!
Onions contains a lot of Hydrogen Sulfide..
Hydrogen sulfide modulates the release of nitric oxide and VEGF in human keratinocytes.
Merighi S, Gessi S, Varani K, Fazzi D, Borea PA.
Source
Department of Clinical and Experimental Medicine, Pharmacology Section and Interdisciplinary Center for the Study of Inflammation, University of Ferrara, Via Fossato di Mortara, 17/19, 44100 Ferrara, Italy.
Abstract
Hydrogen sulfide (H(2)S) is a novel signaling molecule with both pro- or anti-inflammatory effect. The present study aimed to: (i) characterize the in vitro effects of H(2)S on human keratinocyte's proliferation and death; (ii) investigate the ability of H(2)S to modulate VEGF and NO production; (iii) examine the intracellular signaling pathways involved in VEGF and NO modulatory effect. We found that exogenous application of H(2)S (NaHS and GYY4137 as H(2)S donors) significantly enhances NO through increase of iNOS, in a manner Akt-dependent. The increment in NO down-regulates ERK1/2 activation thereby resulting in the decrease of VEGF release. We suggest that H(2)S-releasing agents may be promising therapeutics for chronic inflammatory disorders of the skin, i.e. psoriasis, in which NO increases as well as anti-VEGF treatments have been suggested to be novel effective approaches.
Copyright © 2012 Elsevier Ltd. All rights reserved.
ydrogen sulfide impairs keratinocyte cell growth and adhesion inhibiting mitogen-activated protein kinase signaling.
Gobbi G, Ricci F, Malinverno C, Carubbi C, Pambianco M, Panfilis Gd, Vitale M, Mirandola P.
Source
Department of Anatomy, Pharmacology and Forensic Medicine, University of Parma, Parma, Italy.
Abstract
The effects of exogenous hydrogen sulfide (H2S) on normal skin-derived immortalized human keratinocytes have been investigated in detail. We show in vitro that exogenous hydrogen sulfide reduces clonal growth, cell proliferation and cell adhesion of human keratinocytes. H(2)S, in fact, decreases the frequency of the putative keratinocyte stem cell subpopulation in culture, consequently affecting clonal growth, and impairs cell proliferation and adhesion of mature cells. As a mechanistic explanation of these effects, we show at the molecular level that (i) H2S reduces the Raf/MAPK kinase/ERK signaling pathway; (ii) the reduced adhesion of sulfur-treated cells is associated to the downregulation of the expression of beta4, alpha2 and alpha6 integrins that are necessary to promote cell adhesion as well as anti-apoptotic and proliferative signaling in normal keratinocytes. One specific interest of the effects of sulfurs on keratinocytes derives from the potential applications of the results, as sulfur is able to penetrate the skin and a sulfur-rich balneotherapy has been known for long to be effective in the treatment of psoriasis. Thus, the relevance of our findings to the pathophysiology of psoriasis was tested in vivo by treating psoriatic lesions with sulfurs at a concentration comparable to that most commonly found in sulfurous natural springs. In agreement with the in vitro observations, the immunohistochemical analysis of patient biopsies showed a specific downregulation of ERK activation levels, the key molecular event in the sulfur-induced effects on keratinocytes.
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http://www.pnas.org/content/early/2009/12/01/0908047106.full.pdf
. In animal models of criticalillness, H2S donors protect from lethal hypoxia and reperfusion
injury (3, 8, 9) and exert anti-inflammatory effects (10).
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This is pretty interesting. Couldnt you make a nice shampoo from tea tree, onions, apples, etc and then put it on the scalp right before you go into the shower and use nizoral..... DOUBLE WHAMMY!
The nizoral is some strong stuff and would prob nutrilize the smells pretty quick.
I might be into this since we ended up with an ABUNDANCE of onions at the house somehow and my juicer is right there.
The nizoral is some strong stuff and would prob nutrilize the smells pretty quick.
I might be into this since we ended up with an ABUNDANCE of onions at the house somehow and my juicer is right there.
saintsfan92344
Established Member
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I cant say anything about hair growth because of the 2 times I have used onions but I used it on the sides where I had grey coming in also and buzzed my hair below a 1 and the grey is almost gone on those areas that had the most greys, and that's in 2 weeks of growth, its a noticeable difference, so it may not grow hait but it makes grey hair less noticeable. something at least so I will take it
squeegee
Banned
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[h=1]Hydrogen sulfide mediates the vasoactivity of garlic.[/h]Benavides GA, Squadrito GL, Mills RW, Patel HD, Isbell TS, Patel RP, Darley-Usmar VM, Doeller JE, Kraus DW.
[h=3]Source[/h]Departments of Environmental Health Sciences, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
[h=3]Abstract[/h]The consumption of garlic is inversely correlated with the progression of cardiovascular disease, although the responsible mechanisms remain unclear. Here we show that human RBCs convert garlic-derived organic polysulfides into hydrogen sulfide (H(2)S), an endogenous cardioprotective vascular cell signaling molecule. This H(2)S production, measured in real time by a novel polarographic H(2)S sensor, is supported by glucose-maintained cytosolic glutathione levels and is to a large extent reliant on reduced thiols in or on the RBC membrane. H(2)S production from organic polysulfides is facilitated by allyl substituents and by increasing numbers of tethering sulfur atoms. Allyl-substituted polysulfides undergo nucleophilic substitution at the alpha carbon of the allyl substituent, thereby forming a hydropolysulfide (RS(n)H), a key intermediate during the formation of H(2)S. Organic polysulfides (R-S(n)-R'; n > 2) also undergo nucleophilic substitution at a sulfur atom, yielding RS(n)H and H(2)S. Intact aorta rings, under physiologically relevant oxygen levels, also metabolize garlic-derived organic polysulfides to liberate H(2)S. The vasoactivity of garlic compounds is synchronous with H(2)S production, and their potency to mediate relaxation increases with H(2)S yield, strongly supporting our hypothesis that H(2)S mediates the vasoactivity of garlic. Our results also suggest that the capacity to produce H(2)S can be used to standardize garlic dietary supplements.
[h=1]Hydrogen sulfide mediates the anti-survival effect of sulforaphane on human prostate cancer cells.[/h]Pei Y, Wu B, Cao Q, Wu L, Yang G.
[h=3]Source[/h]Department of Biology, Lakehead University, Thunder Bay, Canada.
[h=3]Abstract[/h]Hydrogen sulfide (H(2)S) is a novel gasotransmitter that regulates cell proliferation and other cellular functions. Sulforaphane (SFN) is a sulfur-containing compound that exhibits anticancer properties, and young sprouts of broccoli are particularly rich in SFN. There is consistent epidemiological evidence that the consumption of sulfur-containing vegetables, such as garlic and cruciferous vegetables, may help reduce the occurrence of prostate cancer. Here we found that a large amount of H(2)S is released when SFN is added into cell culture medium or mixed with mouse liver homogenates, respectively. Both SFN and NaHS (a H(2)S donor) decreased the viability of PC-3 cells (a human prostate cancer cell line) in a dose-dependent manner, and supplement of methemoglobin or oxidized glutathione (two H(2)S scavengers) reversed SFN-reduced cell viability. We further found both cystathionine gamma-lyase (CSE) and cystathionine beta-synthase are expressed in PC-3 cells and mouse prostate tissues. H(2)S production in prostate tissues from CSE knockout mice was only 20% of that from wild-type mice, suggesting CSE is a major H(2)S-producing enzyme in prostate. CSE overexpression enhanced H(2)S production and inhibited cell viability in PC-3 cells. In addition, both SFN and NaHS activated p38 mitogen-activated protein kinases (MAPK) and c-Jun N-terminal kinase (JNK). Pre-treatment of PC-3 cells with methemoglobin decreased SFN-stimulated MAPK activities. Suppression of both p38 MAPK and JNK reversed H(2)S- or SFN-reduced viability of PC-3 cells. Our results demonstrated that H(2)S mediates the inhibitory effect of SFN on the proliferation of PC-3 cells, which suggests that H(2)S-releasing diet or drug might be beneficial in the treatment of prostate cancer.
Copyright © 2011 Elsevier Inc. All rights reserved.
[h=3]Source[/h]Departments of Environmental Health Sciences, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
[h=3]Abstract[/h]The consumption of garlic is inversely correlated with the progression of cardiovascular disease, although the responsible mechanisms remain unclear. Here we show that human RBCs convert garlic-derived organic polysulfides into hydrogen sulfide (H(2)S), an endogenous cardioprotective vascular cell signaling molecule. This H(2)S production, measured in real time by a novel polarographic H(2)S sensor, is supported by glucose-maintained cytosolic glutathione levels and is to a large extent reliant on reduced thiols in or on the RBC membrane. H(2)S production from organic polysulfides is facilitated by allyl substituents and by increasing numbers of tethering sulfur atoms. Allyl-substituted polysulfides undergo nucleophilic substitution at the alpha carbon of the allyl substituent, thereby forming a hydropolysulfide (RS(n)H), a key intermediate during the formation of H(2)S. Organic polysulfides (R-S(n)-R'; n > 2) also undergo nucleophilic substitution at a sulfur atom, yielding RS(n)H and H(2)S. Intact aorta rings, under physiologically relevant oxygen levels, also metabolize garlic-derived organic polysulfides to liberate H(2)S. The vasoactivity of garlic compounds is synchronous with H(2)S production, and their potency to mediate relaxation increases with H(2)S yield, strongly supporting our hypothesis that H(2)S mediates the vasoactivity of garlic. Our results also suggest that the capacity to produce H(2)S can be used to standardize garlic dietary supplements.
[h=1]Hydrogen sulfide mediates the anti-survival effect of sulforaphane on human prostate cancer cells.[/h]Pei Y, Wu B, Cao Q, Wu L, Yang G.
[h=3]Source[/h]Department of Biology, Lakehead University, Thunder Bay, Canada.
[h=3]Abstract[/h]Hydrogen sulfide (H(2)S) is a novel gasotransmitter that regulates cell proliferation and other cellular functions. Sulforaphane (SFN) is a sulfur-containing compound that exhibits anticancer properties, and young sprouts of broccoli are particularly rich in SFN. There is consistent epidemiological evidence that the consumption of sulfur-containing vegetables, such as garlic and cruciferous vegetables, may help reduce the occurrence of prostate cancer. Here we found that a large amount of H(2)S is released when SFN is added into cell culture medium or mixed with mouse liver homogenates, respectively. Both SFN and NaHS (a H(2)S donor) decreased the viability of PC-3 cells (a human prostate cancer cell line) in a dose-dependent manner, and supplement of methemoglobin or oxidized glutathione (two H(2)S scavengers) reversed SFN-reduced cell viability. We further found both cystathionine gamma-lyase (CSE) and cystathionine beta-synthase are expressed in PC-3 cells and mouse prostate tissues. H(2)S production in prostate tissues from CSE knockout mice was only 20% of that from wild-type mice, suggesting CSE is a major H(2)S-producing enzyme in prostate. CSE overexpression enhanced H(2)S production and inhibited cell viability in PC-3 cells. In addition, both SFN and NaHS activated p38 mitogen-activated protein kinases (MAPK) and c-Jun N-terminal kinase (JNK). Pre-treatment of PC-3 cells with methemoglobin decreased SFN-stimulated MAPK activities. Suppression of both p38 MAPK and JNK reversed H(2)S- or SFN-reduced viability of PC-3 cells. Our results demonstrated that H(2)S mediates the inhibitory effect of SFN on the proliferation of PC-3 cells, which suggests that H(2)S-releasing diet or drug might be beneficial in the treatment of prostate cancer.
Copyright © 2011 Elsevier Inc. All rights reserved.
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Regarding Hidrogen sulfide
http://www.ncbi.nlm.nih.gov/pubmed/23297346
Mol Cell Biol. 2013 Mar;33(6):1104-13. doi: 10.1128/MCB.01215-12. Epub 2013 Jan 7.
[h=1]Hydrogen sulfide, the next potent preventive and therapeutic agent in aging and age-associated diseases.[/h]Zhang Y, Tang ZH, Ren Z, Qu SL, Liu MH, Liu LS, Jiang ZS.
[h=3]Source[/h]Institute of Cardiovascular Disease and Key Lab for Arteriosclerology of Hunan Province, University of South China, Hengyang City, Hunan Province, People's Republic of China.
[h=3]Abstract[/h]Hydrogen sulfide (H(2)S) is the third endogenous signaling gasotransmitter, following nitric oxide and carbon monoxide. It is physiologically generated by cystathionine-γ-lyase, cystathionine-β-synthase, and 3-mercaptopyruvate sulfurtransferase. H(2)S has been gaining increasing attention as an important endogenous signaling molecule because of its significant effects on the cardiovascular and nervous systems. Substantial evidence shows that H(2)S is involved in aging by inhibiting free-radical reactions, activating SIRT1, and probably interacting with the age-related gene Klotho. Moreover, H(2)S has been shown to have therapeutic potential in age-associated diseases. This article provides an overview of the physiological functions and effects of H(2)S in aging and age-associated diseases, and proposes the potential health and therapeutic benefits of H(2)S.
http://www.ncbi.nlm.nih.gov/pubmed/23297346
Mol Cell Biol. 2013 Mar;33(6):1104-13. doi: 10.1128/MCB.01215-12. Epub 2013 Jan 7.
[h=1]Hydrogen sulfide, the next potent preventive and therapeutic agent in aging and age-associated diseases.[/h]Zhang Y, Tang ZH, Ren Z, Qu SL, Liu MH, Liu LS, Jiang ZS.
[h=3]Source[/h]Institute of Cardiovascular Disease and Key Lab for Arteriosclerology of Hunan Province, University of South China, Hengyang City, Hunan Province, People's Republic of China.
[h=3]Abstract[/h]Hydrogen sulfide (H(2)S) is the third endogenous signaling gasotransmitter, following nitric oxide and carbon monoxide. It is physiologically generated by cystathionine-γ-lyase, cystathionine-β-synthase, and 3-mercaptopyruvate sulfurtransferase. H(2)S has been gaining increasing attention as an important endogenous signaling molecule because of its significant effects on the cardiovascular and nervous systems. Substantial evidence shows that H(2)S is involved in aging by inhibiting free-radical reactions, activating SIRT1, and probably interacting with the age-related gene Klotho. Moreover, H(2)S has been shown to have therapeutic potential in age-associated diseases. This article provides an overview of the physiological functions and effects of H(2)S in aging and age-associated diseases, and proposes the potential health and therapeutic benefits of H(2)S.
squeegee
Banned
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Regulatory effects of sulfur dioxide on the development of atherosclerotic lesions and vascular hydrogen sulfide in atherosclerotic rats.
Li W, Tang C, Jin H, Du J.
Source
Department of Pediatrics, Peking University First Hospital, Beijing 100034, China.
Abstract
OBJECTIVE:
This study was designed to examine the effect of sulfur dioxide (SO(2)) on atherosclerotic progression and endogenous vascular hydrogen sulfide (H(2)S) in rats with atherosclerosis (AS).
METHODS:
Twenty-eight male rats were randomly divided into control, AS and AS+SO(2) groups. Rats were given a single dose of vitamin D(3) and fed a high-cholesterol diet for 8 weeks to induce AS. Plasma lipids, aortic ultrastructure, and atherosclerotic lesions were detected at the termination of experiment. Plasma and aortic SO(2) were measured using high-performance liquid chromatography, and aspartate aminotransferase (AAT) 1 and AAT2 mRNAs were detected by real-time PCR. Plasma and aortic H(2)S levels were determined with a sulfide-sensitive electrode. Cystathionine-γ-lyase (CSE) mRNA and protein expression was detected. Plasma glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities, malondialdehyde (MDA) and nitric oxide (NO) contents, inducible NO synthase (iNOS) and eNOS activities, and aortic SOD1 and SOD2 expressions were detected.
RESULTS:
Marked atherosclerotic lesions with elevated levels of TC and LDL-C were observed in AS rats. While, there were decreased plasma SO(2) levels and aortic SO(2) production, with a reduced aortic AAT activity in atherosclerotic rats. Plasma GSH-Px and SOD activities were decreased but MDA level increased. Plasma NO content and iNOS activity were also increased. SO(2) donor, however, significantly decreased the atherosclerotic lesions with an increased aortic H(2)S/CSE pathway. It elevated plasma GSH-Px and SOD activities, reduced plasma MDA level, and increased NO/NOS pathway.
CONCLUSIONS:
SO(2) has a marked anti-atherogenic effect with an increase in endogenous H(2)S production in rats with AS.
Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.
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mpact of sulfur dioxide on hydrogen sulfide/cystathionine-γ-lyase and hydrogen sulfide/mercaptopyruvate sulfurtransferase pathways in the pathogenesis of hypoxic pulmonary hypertension in rats].
Authors
Chen SY, et al. Show all Journal
Zhonghua Er Ke Za Zhi. 2011 Dec;49(12):890-4. Article in Chinese.
Affiliation
Department of Pediatrics, Peking University First Hospital, Beijing 100034, China.
Abstract
OBJECTIVE: To explore the impact of sulfur dioxide (SO(2)) on hydrogen sulfide (H(2)S)/cystathionine-γ-lyase (CSE) and H(2)S/mercaptopyruvate sulfurtransferase (MPST) pathways in the pathogenesis of hypoxic pulmonary hypertension.
METHODS: Thirty-two male Wistar rats were randomly divided into four groups: control group (n = 8), hypoxic group (n = 8), hypoxic + SO(2) group (n = 8) and hypoxic + hydroxamate (HDX) group (n = 8). After 21 days of experiment, the concentration and production of H(2)S in lung tissues were measured respectively for each rat. The protein expression of CSE and MPST in intima and media of small pulmonary arteries in rats was detected with immunohistochemical method.
RESULTS: Compared with control group, the mean pulmonary artery pressure (mPAP) in rats of hypoxic group was increased significantly [(33.38 ± 6.32) mm Hg vs. (16.74 ± 3.81) mm Hg, P < 0.01]. Compared with hypoxic group, the mPAP in rats of hypoxic + SO(2) group was decreased significantly [(29.65 ± 2.53) mm Hg vs. (33.38 ± 6.32) mm Hg, P < 0.01]. However, compared with hypoxic group, the mPAP in rats of hypoxic + HDX group was increased significantly [(39.44 ± 6.26) mm Hg vs. (33.38 ± 6.32) mm Hg, P < 0.01]. Compared with control group, the concentration [(2.02 ± 0.43) µmol/g vs. (3.11 ± 0.42) µmol/g, P < 0.01] and production [(19.64 ± 3.48) nmol/(g·min)vs. (28.20 ± 5.95) nmol/(g·min), P < 0.05] of H(2)S were decreased significantly in rats of hypoxic group, respectively. When treated with SO(2), hypoxic rats showed an increased concentration [(2.73 ± 0.20) µmol/g vs. (2.02 ± 0.43) µmol/g, P < 0.01] and production [(26.24 ± 1.92) nmol/(g·min) vs. (19.64 ± 3.48) nmol/(g·min), P < 0.01] of H(2)S in lung tissue compared with those without receiving SO(2) treatment. When treated with HDX, hypoxic rats showed a significant decrease in concentration [(1.64 ± 0.23) µmol/g vs. (2.02 ± 0.43) µmol/g, P < 0.05] and production [(13.94 ± 3.63) nmol/(g·min) vs. (19.64 ± 3.48) nmol/(g·min), P < 0.05] of H(2)S in lung tissue compared with those without receiving HDX treatment. As for the expression of CSE in small pulmonary arteries (SPAs), compared with control group, the expression of CSE in intima [(0.31 ± 0.02) vs. (0.36 ± 0.01), P < 0.01] and media [(0.27 ± 0.01) vs. (0.30 ± 0.01), P < 0.01] in rats of hypoxic group was decreased significantly. While compared with hypoxic group, the expression of CSE in intima [(0.35 ± 0.02) vs. (0.31 ± 0.02), P < 0.01] in SPAs of hypoxic + SO(2) group was increased significantly. With HDX treatment, the expression of CSE in intima [(0.26 ± 0.01) vs. (0.31 ± 0.02), P < 0.01] in SPAs of hypoxic group was lower than that without HDX treatment. As for the expression of MPST in SPAs, compared with hypoxic group, the expression of MPST in media [(0.32 ± 0.02) vs. (0.29 ± 0.01), P < 0.01] in SPAs of hypoxic + SO(2) group was increased significantly.
CONCLUSION: SO(2) might upregulate H(2)S/CSE and H(2)S/MPST pathways in pulmonary arteries of hypoxic rats.
Li W, Tang C, Jin H, Du J.
Source
Department of Pediatrics, Peking University First Hospital, Beijing 100034, China.
Abstract
OBJECTIVE:
This study was designed to examine the effect of sulfur dioxide (SO(2)) on atherosclerotic progression and endogenous vascular hydrogen sulfide (H(2)S) in rats with atherosclerosis (AS).
METHODS:
Twenty-eight male rats were randomly divided into control, AS and AS+SO(2) groups. Rats were given a single dose of vitamin D(3) and fed a high-cholesterol diet for 8 weeks to induce AS. Plasma lipids, aortic ultrastructure, and atherosclerotic lesions were detected at the termination of experiment. Plasma and aortic SO(2) were measured using high-performance liquid chromatography, and aspartate aminotransferase (AAT) 1 and AAT2 mRNAs were detected by real-time PCR. Plasma and aortic H(2)S levels were determined with a sulfide-sensitive electrode. Cystathionine-γ-lyase (CSE) mRNA and protein expression was detected. Plasma glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities, malondialdehyde (MDA) and nitric oxide (NO) contents, inducible NO synthase (iNOS) and eNOS activities, and aortic SOD1 and SOD2 expressions were detected.
RESULTS:
Marked atherosclerotic lesions with elevated levels of TC and LDL-C were observed in AS rats. While, there were decreased plasma SO(2) levels and aortic SO(2) production, with a reduced aortic AAT activity in atherosclerotic rats. Plasma GSH-Px and SOD activities were decreased but MDA level increased. Plasma NO content and iNOS activity were also increased. SO(2) donor, however, significantly decreased the atherosclerotic lesions with an increased aortic H(2)S/CSE pathway. It elevated plasma GSH-Px and SOD activities, reduced plasma MDA level, and increased NO/NOS pathway.
CONCLUSIONS:
SO(2) has a marked anti-atherogenic effect with an increase in endogenous H(2)S production in rats with AS.
Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.
- - - Updated - - -
mpact of sulfur dioxide on hydrogen sulfide/cystathionine-γ-lyase and hydrogen sulfide/mercaptopyruvate sulfurtransferase pathways in the pathogenesis of hypoxic pulmonary hypertension in rats].
Authors
Chen SY, et al. Show all Journal
Zhonghua Er Ke Za Zhi. 2011 Dec;49(12):890-4. Article in Chinese.
Affiliation
Department of Pediatrics, Peking University First Hospital, Beijing 100034, China.
Abstract
OBJECTIVE: To explore the impact of sulfur dioxide (SO(2)) on hydrogen sulfide (H(2)S)/cystathionine-γ-lyase (CSE) and H(2)S/mercaptopyruvate sulfurtransferase (MPST) pathways in the pathogenesis of hypoxic pulmonary hypertension.
METHODS: Thirty-two male Wistar rats were randomly divided into four groups: control group (n = 8), hypoxic group (n = 8), hypoxic + SO(2) group (n = 8) and hypoxic + hydroxamate (HDX) group (n = 8). After 21 days of experiment, the concentration and production of H(2)S in lung tissues were measured respectively for each rat. The protein expression of CSE and MPST in intima and media of small pulmonary arteries in rats was detected with immunohistochemical method.
RESULTS: Compared with control group, the mean pulmonary artery pressure (mPAP) in rats of hypoxic group was increased significantly [(33.38 ± 6.32) mm Hg vs. (16.74 ± 3.81) mm Hg, P < 0.01]. Compared with hypoxic group, the mPAP in rats of hypoxic + SO(2) group was decreased significantly [(29.65 ± 2.53) mm Hg vs. (33.38 ± 6.32) mm Hg, P < 0.01]. However, compared with hypoxic group, the mPAP in rats of hypoxic + HDX group was increased significantly [(39.44 ± 6.26) mm Hg vs. (33.38 ± 6.32) mm Hg, P < 0.01]. Compared with control group, the concentration [(2.02 ± 0.43) µmol/g vs. (3.11 ± 0.42) µmol/g, P < 0.01] and production [(19.64 ± 3.48) nmol/(g·min)vs. (28.20 ± 5.95) nmol/(g·min), P < 0.05] of H(2)S were decreased significantly in rats of hypoxic group, respectively. When treated with SO(2), hypoxic rats showed an increased concentration [(2.73 ± 0.20) µmol/g vs. (2.02 ± 0.43) µmol/g, P < 0.01] and production [(26.24 ± 1.92) nmol/(g·min) vs. (19.64 ± 3.48) nmol/(g·min), P < 0.01] of H(2)S in lung tissue compared with those without receiving SO(2) treatment. When treated with HDX, hypoxic rats showed a significant decrease in concentration [(1.64 ± 0.23) µmol/g vs. (2.02 ± 0.43) µmol/g, P < 0.05] and production [(13.94 ± 3.63) nmol/(g·min) vs. (19.64 ± 3.48) nmol/(g·min), P < 0.05] of H(2)S in lung tissue compared with those without receiving HDX treatment. As for the expression of CSE in small pulmonary arteries (SPAs), compared with control group, the expression of CSE in intima [(0.31 ± 0.02) vs. (0.36 ± 0.01), P < 0.01] and media [(0.27 ± 0.01) vs. (0.30 ± 0.01), P < 0.01] in rats of hypoxic group was decreased significantly. While compared with hypoxic group, the expression of CSE in intima [(0.35 ± 0.02) vs. (0.31 ± 0.02), P < 0.01] in SPAs of hypoxic + SO(2) group was increased significantly. With HDX treatment, the expression of CSE in intima [(0.26 ± 0.01) vs. (0.31 ± 0.02), P < 0.01] in SPAs of hypoxic group was lower than that without HDX treatment. As for the expression of MPST in SPAs, compared with hypoxic group, the expression of MPST in media [(0.32 ± 0.02) vs. (0.29 ± 0.01), P < 0.01] in SPAs of hypoxic + SO(2) group was increased significantly.
CONCLUSION: SO(2) might upregulate H(2)S/CSE and H(2)S/MPST pathways in pulmonary arteries of hypoxic rats.
waynakyo
Experienced Member
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I have nothing to gain from saying this except I would love to see another success story like me on OC. I was dumbfounded and still by the fact that it has COMPLETELY stopped my shedding, for a longer period than I have ever experienced since before my hairloss. It is pricey, but if shedding is bothering you and you can afford it try OC. it has no side effects except mild insomnia and it has been tried on humans before. good luck.
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By the way guys it is a well known facts that onion juice is used as a "home remedy" for alopecia aerata. I had 2 spots that came up on my beard 3-4 years ago, I applied onion juice for about a month and they completely regrew. No trace. This alone is not a proof since AA sometimes is transitory. HOwever I have seen studies for onion juice in AA cases being successful to some degree.