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Michael Guppy - One of the best experts on this subject based on the ideXlab platform.
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do australian desert frogs co accumulate counteracting solutes with urea during aestivation
The Journal of Experimental Biology, 1996Co-Authors: Philip C Withers, Michael GuppyAbstract:Australian desert frogs of the genera Neobatrachus, Cyclorana and Heleioporus experience significant dehydration, and iono- and osmoconcentration, during aestivation in the laboratory and accumulate substantial amounts of urea (100-200 mmol)(l-1). We expected a priori that aestivating frogs probably would not need to accumulate balancing osmolytes but would accumulate Trimethylamine Oxide (TMAO) or betaine as counteracting solutes to urea. These aestivating frogs did not co-accumulate a substantial quantity of any particular balancing osmolyte or counteracting solute, such as a methylamine [TMAO, Trimethylamine amine (TMA), betaine, sarcosine, glycerophosphorylcholine (GPC)] or polyol (inositol, mannitol, sorbitol) in plasma or muscle relative to urea accumulation. However, for aestivating frogs, the total concentration of all measured methylamines and polyols (TMAO + TMA + betaine + sarcosine + GPC + inositol) in muscle was approximately 35-45 mmol kg-1, and so it is possible that all of these solutes have a combined counteracting osmolyte role in aestivating frogs at a ratio to urea of approximately 1:2.5, as has been described for elasmobranch fishes. Alternatively, the absence of substantial co-accumulation with urea of any particular solute suggests that aestivating frogs might not require any major extracellular or intracellular counteracting solutes (TMAO, betaine, GPC). The enzyme systems of these aestivating frogs may be insensitive to the perturbing effects of urea, or the perturbing effects of accumulated urea may be a mechanism for metabolic depression, during aestivation.
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buoyancy role of urea and tmao in an elasmobranch fish the port jackson shark heterodontus portusjacksoni
Physiological and Biochemical Zoology, 1994Co-Authors: Philip C Withers, Garrick Morrison, Michael GuppyAbstract:The Port Jackson shark is denser than seawater, like most other elasmobranchs. Its small liver, of relatively low lipid content, does not contribute significantly to buoyancy. Like other elasmobranchs, Port Jackson sharks accumulate high levels of urea and methylamines (Trimethylamine Oxide [TMAO] and betaine) in their body fluids as important balancing osmolytes. We calculate from the solute composition of plasma and muscle fluid, using molecular weights and partial molal volumes of solutes, that urea and TMAO in the body fluids of the Port Jackson shark contribute significant positive buoyancy. The high, positive partial molal volumes of urea, TMAO, and betaine provide this positive buoyancy despite their high molecular weights. The accounted solutes in plasma provide a net lift of about 2. 4 g L⁻¹ relative to seawater; positive lift is contributed by CI⁻ (3.6 g L⁻¹), urea (2.8 g L⁻¹), and TMAO (1. 7g L⁻¹), and negative lift is contributed by Na⁺ (-1.8 g L⁻¹) and protein (-3.5 g L⁻¹). For muscle fluid, ...
Gabriel G Haddad - One of the best experts on this subject based on the ideXlab platform.
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intermittent hypoxia and hypercapnia accelerate atherosclerosis partially via Trimethylamine Oxide
American Journal of Respiratory Cell and Molecular Biology, 2017Co-Authors: Jin Xue, Dan Zhou, Orit Poulsen, Toshihiro Imamura, Yuhsin Hsiao, Travis H Smith, Atul Malhotra, Pieter C Dorrestein, Rob Knight, Gabriel G HaddadAbstract:Obstructive sleep apnea (OSA) is a common disorder characterized by intermittent hypoxia and hypercapnia (IHC) during sleep. OSA has been shown to be a risk factor for atherosclerosis, but the relation of IHC to the induction or progression of atherosclerosis is not well understood. To dissect the mechanisms involved, we compared atherosclerotic lesion formation in two mouse models, i.e., apolipoprotein E (ApoE) and low density lipoprotein receptor (Ldlr)-deficient mice, with or without IHC exposure. Ten-week-old ApoE-/- or Ldlr-/- mice were fed a high-fat diet for 4 or 8 weeks while being exposed to IHC for 10 hours/day or room air (RA) for 24 hours/day. En face lesions of the aorta, aortic arch, and pulmonary artery (PA) were examined. Moreover, 3,3-dimethyl-1-butanol (DMB), an inhibitor of microbial Trimethylamine (TMA) production, was used to determine the contribution of TMA-Oxide (TMAO) to IHC-induced atherosclerosis. Eight weeks of IHC exposure expedited the formation of atherosclerosis in both the PA and aortic arch of ApoE-/- mice, but only in the PA of Ldlr-/- mice (ApoE-/- PA 8 wk, IHC 35.4 ± 1.9% versus RA 8.0 ± 2.8%, P < 0.01). The atherosclerotic lesions evolved faster and to a more severe extent in ApoE-/- mice as compared with Ldlr-/- mice (PA IHC 8 wk, ApoE-/- 35.4 ± 1.9% versus Ldlr-/- 8.2 ± 1.5%, P < 0.01). DMB significantly attenuated but did not totally eliminate IHC-induced PA atherosclerosis. Our findings suggest that IHC, a hallmark of OSA, accelerates the progression of atherosclerosis in the aorta and especially in the PA. This process is partly inhibited by DMB, demonstrating that microbial metabolites may serve as therapeutic targets for OSA-induced atherosclerosis.
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intermittent hypoxia and hypercapnia accelerate atherosclerosis partially via Trimethylamine Oxide
American Journal of Respiratory Cell and Molecular Biology, 2017Co-Authors: Dan Zhou, Orit Poulsen, Toshihiro Imamura, Yuhsin Hsiao, Travis H Smith, Atul Malhotra, Pieter C Dorrestein, Rob Knight, Gabriel G HaddadAbstract:Obstructive sleep apnea (OSA) is a common disorder characterized by intermittent hypoxia and hypercapnia (IHC) during sleep. OSA has been shown to be a risk factor for atherosclerosis, but the relation of IHC to the induction or progression of atherosclerosis is not well understood. To dissect the mechanisms involved, we compared atherosclerotic lesion formation in two mouse models, i.e., apolipoprotein E (ApoE) and low density lipoprotein receptor (Ldlr)–deficient mice, with or without IHC exposure. Ten-week-old ApoE−/− or Ldlr−/− mice were fed a high-fat diet for 4 or 8 weeks while being exposed to IHC for 10 hours/day or room air (RA) for 24 hours/day. En face lesions of the aorta, aortic arch, and pulmonary artery (PA) were examined. Moreover, 3,3-dimethyl-1-butanol (DMB), an inhibitor of microbial Trimethylamine (TMA) production, was used to determine the contribution of TMA-Oxide (TMAO) to IHC-induced atherosclerosis. Eight weeks of IHC exposure expedited the formation of atherosclerosis in both the...
Suzanne Currie - One of the best experts on this subject based on the ideXlab platform.
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physiological responses to hypersalinity correspond to nursery ground usage in two inshore shark species mustelus antarcticus and galeorhinus galeus
The Journal of Experimental Biology, 2016Co-Authors: Louise Tunnah, Sara R C Mackellar, David A Barnett, Tyson J Maccormack, Kilian M Stehfest, Andrea J Morash, Jayson M Semmens, Suzanne CurrieAbstract:ABSTRACT Shark nurseries are susceptible to environmental fluctuations in salinity because of their shallow, coastal nature; however, the physiological impacts on resident elasmobranchs are largely unknown. Gummy sharks (Mustelus antarcticus) and school sharks (Galeorhinus galeus) use the same Tasmanian estuary as a nursery ground; however, each species has distinct distribution patterns that are coincident with changes in local environmental conditions, such as increases in salinity. We hypothesized that these differences were directly related to differential physiological tolerances to high salinity. To test this hypothesis, we exposed wild, juvenile school and gummy sharks to an environmentally relevant hypersaline (120% SW) event for 48 h. Metabolic rate decreased 20–35% in both species, and gill Na+/K+-ATPase activity was maintained in gummy sharks but decreased 37% in school sharks. We measured plasma ions (Na+, K+, Cl−) and osmolytes [urea and Trimethylamine Oxide (TMAO)], and observed a 33% increase in plasma Na+ in gummy sharks with hyperosmotic exposure, while school sharks displayed a typical ureosmotic increase in plasma urea (∼20%). With elevated salinity, gill TMAO concentration increased by 42% in school sharks and by 30% in gummy sharks. Indicators of cellular stress (heat shock proteins HSP70, 90 and 110, and ubiquitin) significantly increased in gill and white muscle in both a species- and a tissue-specific manner. Overall, gummy sharks exhibited greater osmotic perturbation and ionic dysregulation and a larger cellular stress response compared with school sharks. Our findings provide physiological correlates to the observed distribution and movement of these shark species in their critical nursery grounds.
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chaperone roles for tmao and hsp70 during hyposmotic stress in the spiny dogfish shark squalus acanthias
Journal of Comparative Physiology B-biochemical Systemic and Environmental Physiology, 2015Co-Authors: Robyn J Maclellan, Louise Tunnah, David A Barnett, Tyson J Maccormack, Patricia A. Wright, Suzanne CurrieAbstract:Salinity decreases are experienced by many marine elasmobranchs. To understand how these fishes cope with hyposmotic stress on a cellular level, we used the spiny dogfish shark (Squalus acanthias) as a model to test whether a reciprocal relationship exists between the cell’s two primary protein protection mechanisms, the chemical (e.g., Trimethylamine Oxide, TMAO) and molecular (e.g., heat shock protein 70, HSP70) chaperone systems. This relationship is interesting given that many elasmobranchs are expected to gain water and lose osmolytes, chemical chaperones, and ions as they osmoconform to new, lowered salinity. Dogfish were cannulated for repeated blood sampling and exposed to 70 % seawater (SW) for 48 h. These hyposmotic conditions had no effect on red blood cell (RBC) and white muscle TMAO concentrations, and did not result in HSP70 induction or signs of protein damage (i.e., increased ubiquitin), suggesting that TMAO levels were sufficiently protective in these tissues. However, in the gill, we observed a significant decrease in TMAO concentration and a significant induction of HSP70 as well as signs of protein damage. In the face of this cellular stress response, gill Na+/K+-ATPase (NKA) activity significantly increased during hyposmotic conditions, as expected. We suggest that this functional preservation in the gill is partly the result of HSP70 induction with lowered salinity. We conclude a reciprocal relationship between TMAO and HSP70 in the gills of dogfish as a result of in vivo hyposmotic stress. When osmotically induced protein damage surpasses the protective capacity of remaining TMAO, HSP70 is induced to preserve tissue and organismal function.
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coordination of chemical Trimethylamine Oxide and molecular heat shock protein 70 chaperone responses to heat stress in elasmobranch red blood cells
Physiological and Biochemical Zoology, 2014Co-Authors: Ashra Kolhatkar, Cayleih E Robertson, Maria Thistle, Kurt A Gamperl, Suzanne CurrieAbstract:AbstractChemical and molecular chaperones are organic compounds that protect and stabilize proteins from damage and aggregation as a result of cellular stress. Using the dogfish (Squalus acanthias) red blood cell (RBC) as a model, we examined whether elasmobranch cells with naturally high concentrations of the chemical chaperone Trimethylamine Oxide (TMAO) would induce the molecular chaperone heat shock protein 70 (HSP70) when exposed to an acute thermal stress. Our hypothesis was that TMAO is itself capable of preventing damage and preserving cellular function during thermal stress and thus that the heat shock response would be inhibited/diminished. We incubated RBCs in vitro with and without physiologically relevant concentrations of TMAO at 13°C and then exposed cells to a 1-h acute heat shock at 24°C. HSP70 protein expression was elevated in dogfish RBCs after the acute heat stress, but this induction was inhibited by extracellular TMAO. Regardless of the presence of TMAO and/or HSP70, we did not obse...
Philip C Withers - One of the best experts on this subject based on the ideXlab platform.
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do australian desert frogs co accumulate counteracting solutes with urea during aestivation
The Journal of Experimental Biology, 1996Co-Authors: Philip C Withers, Michael GuppyAbstract:Australian desert frogs of the genera Neobatrachus, Cyclorana and Heleioporus experience significant dehydration, and iono- and osmoconcentration, during aestivation in the laboratory and accumulate substantial amounts of urea (100-200 mmol)(l-1). We expected a priori that aestivating frogs probably would not need to accumulate balancing osmolytes but would accumulate Trimethylamine Oxide (TMAO) or betaine as counteracting solutes to urea. These aestivating frogs did not co-accumulate a substantial quantity of any particular balancing osmolyte or counteracting solute, such as a methylamine [TMAO, Trimethylamine amine (TMA), betaine, sarcosine, glycerophosphorylcholine (GPC)] or polyol (inositol, mannitol, sorbitol) in plasma or muscle relative to urea accumulation. However, for aestivating frogs, the total concentration of all measured methylamines and polyols (TMAO + TMA + betaine + sarcosine + GPC + inositol) in muscle was approximately 35-45 mmol kg-1, and so it is possible that all of these solutes have a combined counteracting osmolyte role in aestivating frogs at a ratio to urea of approximately 1:2.5, as has been described for elasmobranch fishes. Alternatively, the absence of substantial co-accumulation with urea of any particular solute suggests that aestivating frogs might not require any major extracellular or intracellular counteracting solutes (TMAO, betaine, GPC). The enzyme systems of these aestivating frogs may be insensitive to the perturbing effects of urea, or the perturbing effects of accumulated urea may be a mechanism for metabolic depression, during aestivation.
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buoyancy role of urea and tmao in an elasmobranch fish the port jackson shark heterodontus portusjacksoni
Physiological and Biochemical Zoology, 1994Co-Authors: Philip C Withers, Garrick Morrison, Michael GuppyAbstract:The Port Jackson shark is denser than seawater, like most other elasmobranchs. Its small liver, of relatively low lipid content, does not contribute significantly to buoyancy. Like other elasmobranchs, Port Jackson sharks accumulate high levels of urea and methylamines (Trimethylamine Oxide [TMAO] and betaine) in their body fluids as important balancing osmolytes. We calculate from the solute composition of plasma and muscle fluid, using molecular weights and partial molal volumes of solutes, that urea and TMAO in the body fluids of the Port Jackson shark contribute significant positive buoyancy. The high, positive partial molal volumes of urea, TMAO, and betaine provide this positive buoyancy despite their high molecular weights. The accounted solutes in plasma provide a net lift of about 2. 4 g L⁻¹ relative to seawater; positive lift is contributed by CI⁻ (3.6 g L⁻¹), urea (2.8 g L⁻¹), and TMAO (1. 7g L⁻¹), and negative lift is contributed by Na⁺ (-1.8 g L⁻¹) and protein (-3.5 g L⁻¹). For muscle fluid, ...
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role of urea and methylamines in buoyancy of elasmobranchs
The Journal of Experimental Biology, 1994Co-Authors: Philip C Withers, G T Hefter, T S PangAbstract:The possible role of urea and Trimethylamine Oxide (TMAO) in providing positive buoyancy has been examined for elasmobranch fishes. TMAO has a considerably lower density than an equimolar solution of urea, and solutions of both TMAO and urea are considerably less dense than equimolar solutions of most other body fluid solutes. The body fluid composition of three elasmobranchs, the whiskery shark Furgaleus ventralis, the black whaler shark Carcharhinus obscurus and the shovelnosed ray Aptychotremata vincentiana, is typical for marine elasmobranchs, with plasma concentrations of about 260 mmol l-1 Na+, 250 mmol l-1 Cl-, 340 mmol l-1 urea and 70 mmol l-1 Trimethylamine Oxide. A plasma density of 1.015 was calculated for the whaler shark (from the concentrations, relative molecular masses and absolute molal volumes of plasma solutes), which would contribute a positive lift of 8.45 g l-1. There is a large positive contribution to buoyancy by urea (3.7 g l-1), Trimethylamine Oxide (1.8 g l-1) and Cl- (4.0 g l-1), whereas slight negative buoyancy is conferred by Na+ (-0.8 g l-1). Divalent cations (Ca2+, Mg2+) contribute minimal negative buoyancy (about -0.1 g l-1 each) despite their rather negative partial molal volumes, because of their low concentrations. Muscle fluids contain about 40 mmol l-1 Cl-, 365 mmol l-1 urea, 160 mmol l-1 Trimethylamine Oxide, 16 mmol l-1 betaine and 69 mmol l-1 sarcosine. The organic solutes contribute about 12.1 g l-1 lift. Although urea and TMAO act as balancing osmolytes, and TMAO as a counteracting solute, a positive buoyancy role must be considered as a further adaptive function of urea and TMAO accumulation in chondrichthyean fishes.
Urban Forsum - One of the best experts on this subject based on the ideXlab platform.
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Trimethylamine and Trimethylamine Oxide levels in normal women and women with bacterial vaginosis reflect a local metabolism in vaginal secretion as compared to urine
Apmis, 2005Co-Authors: Helen Wolrath, Anders Hallen, Bengt Stahlbom, Urban ForsumAbstract:The smell of rotten fish is one of the characteristics of bacterial vaginosis (BV), and is due to Trimethylamine (TMA). Trimethylamine can be found in human urine, although most of it occurs as the nonvolatile Oxide (TMAO) form. The fraction TMA/TMAO can be expected to be the same in different body fluids if no local production of TMA occurs. In women with BV, TMAO in the vaginal fluid is expected to be chemically reduced by the local bacterial flora to the much more odorous TMA. We have therefore studied the local vaginal production of TMA in vaginal secretion compared to the general TMA-TMAO metabolism that was measured in urine using gas chromatography. Both vaginal fluid and random urine samples were collected from women, with and without BV, attending a Swedish clinic for sexually transmitted diseases, and these samples were analyzed for TMA and TMAO. The results show that a local production of TMA occurs in the vagina that is not part of the general metabolism of TMA-TMAO.
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Trimethylamine content in vaginal secretion and its relation to bacterial vaginosis
Apmis, 2002Co-Authors: Helen Wolrath, Hans Boren, Anders Hallen, Urban ForsumAbstract:The presence of a fishy odor emanating from women who present with a malodorous vaginal discharge is well known. The odor is due to bacterial reduction of Trimethylamine Oxide to Trimethylamine (TMA) in vaginal secretion. The release of TMA from specimens of vaginal fluid following the addition of alkali is often used in making a clinical diagnosis of bacterial vaginosis (BV). We now report a sensitive gas chromatographic method for analysis and quantification of TMA in vaginal fluid in which weighed samples were used. In addition, a proper diagnosis of BV was obtained using Gram-stained smears of the vaginal fluid according to the method of Nugent et al. (R. P. Nugent et al., J Clin Microbiol 1991;29:297–301). We also diagnosed BV according to Hallen et al. (A. Hallen et al. Genitourin Med 1987;63:386–9). TMA was present in all women with a Nugent score between 7 and 10 and in almost all women diagnosed with BV according to the method of Hallen et al. TMA was not found or was only found in very low concentrations in vaginal fluid from women with Nugent scores of 0 to 3. TMA was also found in four women with a negative sniff test. It seems that high levels of TMA in samples of vaginal fluid are typical for BV regardless of the scoring method used for diagnosis. However, low levels of TMA, <5 μg/g vaginal fluid, do not always correlate with BV.
