共查询到20条相似文献,搜索用时 15 毫秒
1.
Hydrogen sulfide (H 2S), can produce pharmacological effects on neural and non-neural tissues from several mammalian species. The present study
investigates the pharmacological action of H 2S, (using sodium hydrosulfide, NaHS, and/or sodium sulfide, Na 2S as donors) on amino acid neurotransmission (using [ 3H] d-aspartate as a marker for glutamate) from isolated, superfused bovine and porcine retinae. Isolated neural retinae were incubated
in Krebs solution containing [ 3H] d-aspartate at 37°C. Release of [ 3H] d-aspartate was elicited by high potassium (K + 50 mM) pulse. Both NaHS and Na 2S donors caused an inhibition of K +-evoked [ 3H] d-aspartate release from isolated bovine retinae without affecting basal [ 3H] d-aspartate efflux yielding IC 50 values of 0.006 and 6 μm, respectively. Furthermore, NaHS inhibited depolarization-evoked release of [ 3H] d-aspartate from isolated porcine retinae with an IC 50 value of 8 μM. The inhibitory action of NaHS on [ 3H] d-aspartate release from porcine retinae was blocked by propargyglycine, a selective inhibitor of cystathionine γ-lyase (CSE).
Our results indicate that H 2S donors can inhibit amino acid neurotransmission from both isolated bovine and porcine retinae, an effect that is dependent,
at least in part, on intramural biosynthesis of H 2S. 相似文献
2.
Hydrogen sulfide (H 2S) is a novel gasotransmitter with physiological and pathological functions in vascular homeostasis, cardiovascular system
and central nervous system. In the present study, we determined the endogenous levels of H 2S in various tissues of the bovine eye. We also examined the basal levels of H 2S in response to donors (sodium hydrosulfide, NaHS and sodium sulfide, Na 2S), substrate ( l-cysteine), inhibitors (propargylglycine, PAG and aminooxyacetic acid, AOA) and activator (S-adenosyl- l-methionine, SAM) of this gas in the bovine retina. H 2S was measured using a well established spectrophotometric method. The highest concentration of endogenous H 2S was detected in cornea (19 ± 2.85 nmoles/mg protein, n = 6) and retina (17 ± 2.1 nmoles/mg protein, n = 6). Interestingly, H 2S was not present in vitreous humor. The inhibitors of CSE and CBS; PAG (1 mM) and AOA (1 mM), significantly attenuated the
production of H 2S in the bovine retina by 56.8 and 42%, respectively. On the other hand the activator of CBS; SAM (100 μM), H 2S donors; NaHS (1 μM) and Na 2S (100 μM), significantly increased endogenous levels of H 2S in bovine retina. l-cysteine (10–300 μM) produced a significant ( P < 0.05) concentration-dependent increase in H 2S levels reaching a maximal at 300 μM. We conclude that H 2S is endogenously produced in various tissues of the isolated bovine eye. Moreover, endogenous levels of H 2S are enhanced in the presence of substrate ( l-cysteine), an activator of CBS (SAM) and H 2S donors but are blocked by inhibitors of enzymes that synthesize this gas in neural retina. 相似文献
3.
In the present study, we investigated the pharmacological action of hydrogen sulfide (H 2S, using sodium hydrosulfide, NaHS, and/or sodium sulfide, Na 2S as donors) on sympathetic neurotransmission from isolated, superfused porcine iris-ciliary bodies. We also examined the
effect of H 2S on norepinephrine (NE), dopamine and epinephrine concentrations in isolated porcine anterior uvea. Release of [ 3H]NE was triggered by electrical field stimulation and basal catecholamine concentrations was measured by high performance
liquid chromatography (HPLC). Both NaHS and Na 2S caused a concentration-dependent inhibition of electrically evoked [ 3H]NE release from porcine iris-ciliary body without affecting basal [ 3H]NE efflux. The inhibitory action of H 2S donors on NE release was attenuated by aminooxyacetic acid (AOA) and propargyglycine (PAG), inhibitors of cystathionine
β-synthase (CBS) and cystathionine γ-lyase (CSE), respectively. With the exception of dopamine, NaHS caused a concentration-dependent
reduction in endogenous NE and epinephrine concentrations in isolated iris-ciliary bodies. We conclude that H 2S can inhibit sympathetic neurotransmission from isolated porcine anterior uvea, an effect that is dependent, at least in
part, on intramural biosynthesis of this gas. Furthermore, the observed action of H 2S donors on sympathetic transmission may be due to a direct action of this gas on neurotransmitter pools. 相似文献
4.
The protective properties of a prenylated coumarin, umbelliprenin (UMB), on the human lymphocytes DNA lesions were tested.
Lymphocytes were isolated from blood samples taken from healthy volunteers. DNA breaks and resistance to H 2O 2-induced damage were measured using a single-cell microgel electrophoresis technique under alkaline conditions (comet assay).
Human lymphocytes were incubated in UMB (10, 25, 50, 100, 200, and 400 μM) alone or a combination of different concentrations
of UMB (10, 25, 50, 100, 200, and 400 μM) and 25 μM H 2O 2. Untreated cells, ascorbic acid (AA; 25, 50, 100, 200, and 400 μM) and H 2O 2 (25 μM) were considered as negative control, positive control, and the standard antioxidant agent for our study, respectively.
Single cells were analyzed with “TriTek Cometscore version 1.5” software. The DNA damage was expressed as percent tail DNA.
UMB exhibited a concentration-dependent increase in protection activity against DNA damage induced by 25 μM H 2O 2 (from 67.28% to 39.17%). The antigenotoxic activity of AA, in the range 0–50 μM, was greater than that of UMB. However, no
significant difference ( p > 0.05) in the protective activity was found between UMB and AA at concentrations of approximately higher than 50 μM. 相似文献
5.
Effects of NaHS, H 2S donor, on germination and antioxidant metabolism in wheat ( Triticum aestivum L.) seeds under osmotic stress were investigated. With the enhancement of osmotic stress, which was mimicked by PEG-6000,
the seed germination dropped gradually. NaHS treatment could promote wheat seed germination against osmotic stress in a dose-dependent
manner; while Na + and other sulfur-containing components, such as S 2−, SO 42−, SO 32−, HSO 4− and HSO 3−, were not able to improve seed germination as NaHS did, confirming H 2S or HS − derived from NaHS contribute to the protective roles. Further experiments showed that NaHS treatment combined with PEG enhanced
the activities of amylase and esterase in comparison to PEG treatment alone. Alternatively, NaHS treatment significantly reduced
malondialdehyde and hydrogen peroxide accumulation in seeds. Significant enhancement of catalase and ascorbate peroxidase
activities and decrease in lipoxygenase activity were observed in NaHS treated seeds, while peroxidase and superoxide dismutase
activities were not affected as compared with the control. Furthermore, the H 2S donor treatment could retain higher levels of endogenous H 2S in wheat seeds under osmotic stress. These data indicated that H 2S played a protective role in wheat seed against osmotic stress. 相似文献
6.
Prostaglandin E 2 (PGE 2) is the major vasodilator prostanoid of the mammalian ductus arteriosus (DA). In the present study we analyzed the response
of isolated DA rings from 15-, 19- and 21-day-old chicken embryos to PGE 2 and other vascular smooth muscle relaxing agents acting through the cyclic AMP signaling pathway. PGE 2 exhibited a relaxant response in the 15-day DA, but not in the 19- and 21-day DA. Moreover, high concentrations of PGE 2 (≥3 μM in 15-day and ≥1 μM in 19-day and 21-day DA) induced contraction of the chicken DA. The presence of the TP receptor
antagonist SQ29,548, unmasked a relaxant effect of PGE 2 in the 19- and 21-day DA and increased the relaxation induced by PGE 2 in the 15-day DA. The presence of the EP receptor antagonist AH6809 abolished PGE 2-mediated relaxation. The relaxant responses induced by PGE 2 and the β-adrenoceptor agonist isoproterenol, but not those elicited by the adenylate cyclase activator forskolin or the
phosphodiesterase 3 inhibitor milrinone, decreased with maturation. High oxygen concentrations (95%) decreased the relaxation
to PGE 2. The relaxing potency and efficacy of isoproterenol and milrinone were higher in the pulmonary than in the aortic side of
the DA, whereas no regional differences were found in the response to PGE 2. We conclude that, in contrast to the mammalian situation, PGE 2 is a weak relaxant agent of the chicken DA and, with advancing incubation, it even stimulates TP vasoconstrictive receptors. 相似文献
7.
Hydrogen sulfide (H 2S), a gasotransmitter, is formed from l-cysteine by multiple enzymes including cystathionine-γ-lyase (CSE). We have shown that an H 2S donor, NaHS, causes hyperalgesia in rodents, an effect inhibited by knockdown of Ca v3.2 T-type Ca 2+ channels (T-channels), and that NaHS facilitates T-channel-dependent currents (T-currents) in NG108-15 cells that naturally express Ca v3.2. In the present study, we asked if endogenous and exogenous H 2S participates in regulation of the channel functions in Ca v3.2-transfected HEK293 (Ca v3.2-HEK293) cells. dl-Propargylglycine (PPG), a CSE inhibitor, significantly decreased T-currents in Ca v3.2-HEK293 cells, but not in NG108-15 cells. NaHS at 1.5 mM did not affect T-currents in Ca v3.2-HEK293 cells, but enhanced T-currents in NG108-15 cells. In the presence of PPG, NaHS at 1.5 mM, but not 0.1–0.3 mM, increased T-currents in Ca v3.2-HEK293 cells. Similarly, Na 2S, another H 2S donor, at 0.1–0.3 mM significantly increased T-currents in the presence, but not absence, of PPG in Ca v3.2-HEK293 cells. Expression of CSE was detected at protein and mRNA levels in HEK293 cells. Intraplantar administration of Na 2S, like NaHS, caused mechanical hyperalgesia, an effect blocked by NNC 55-0396, a T-channel inhibitor. The in vivo potency of Na 2S was higher than NaHS. These results suggest that the function of Ca v3.2 T-channels is tonically enhanced by endogenous H 2S synthesized by CSE in Ca v3.2-HEK293 cells, and that exogenous H 2S is capable of enhancing Ca v3.2 function when endogenous H 2S production by CSE is inhibited. In addition, Na 2S is considered a more potent H 2S donor than NaHS in vitro as well as in vivo. 相似文献
8.
A novel amperometric hydrogen peroxide biosensor based on the immobilization of hemoglobin on the 2,6-pyridinedicarboxylic
acid (PDC) polymer, thionine and nano-Au was successfully fabricated. In this strategy, PDC polymer acted as the matrices
to covalently immobilize the thionine, and then hemoglobin was successfully adsorbed on the nano-Au which was electro-deposited
on to thionine modified electrode surface. The preparation process of modified electrode was characterized with electrochemical
impedance spectroscopy and atomic force microscope. The analytical performance of proposed biosensor toward H 2O 2 was investigated by cyclic voltammetry and chronoamperometry. The resulted biosensor exhibited fast amperometric response
(within 6 s) to H 2O 2, and linear range was from 9.1 μM to 5.0 mM with the detection limit of 2.6 μM (S/N = 3). The apparent Michaelis–Menten constant
( K
Mapp) was evaluated to be 3.2 mM. Furthermore, the resulted biosensor showed good stability and reproducibility. 相似文献
9.
We investigated the effect of isoprostanes (IsoPs) on potassium (K +)-depolarization-evoked release of [ 3H]dopamine from isolated bovine retinae. Isolated retinae were preloaded with [ 3H]dopamine and then prepared for studies of [ 3H]dopamine release using the superfusion method. 8-iso(15R)PGF 2α, 8-isoPGE 2, 8-isoPGE 1 and 8-isoPGF 2α attenuated [ 3H]dopamine release from isolated bovine retinae. At a concentration of 1 μM, the rank order of activity displayed by IsoP
agonists was: 8-iso(15R)PGF 2α > 8-isoPGE 2 > 8-isoPGE 1 > 8-isoPGF 2α. Inhibition of cyclooxygenase (COX) with flurbiprofen reversed the effects caused by 8-isoPGE 2 (10 nM and 10 μM), 8-iso(15R)PGF 2α (1 μM) and 8-isoPGE 1 (1 μM). Although the EP1/EP2 antagonist, AH 6809 (10 μM) had no significant effect on K +-induced [ 3H]dopamine release, it blocked the inhibitory effect of both 8-isoPGE 1 (10 μM) and 8-isoPGE 2 (10 μM). In conclusion, IsoPs attenuate K +-induced [ 3H]dopamine release in isolated bovine retinae, presumably via an indirect action on COX pathway leading to the production
of prostanoids, which in turn, activates EP receptors. 相似文献
10.
Diazinon and malathion are commonly used organophosphate insecticides in agriculture, industry, and in veterinary medicine
as an ectoparasiticide. The importance to carry out in vitro reproductive toxicology assays lies on the need of knowing the
alterations these insecticides may cause at cellular level, since they are endocrine disruptors that interfere with reproductive
functions. The aim of this study was to evaluate in vitro oocyte viability, fertilization, and embryo development with different
concentrations of diazinon and malathion. For in vitro fertilization (IVF), porcine oocytes and sperm were co-incubated for
7 h with increasing concentrations (50, 100, and 500 μM) of diazinon and malathion. For embryo development, fertilized oocytes
were cultured in medium containing the same insecticide concentrations during 96 h for embryo development and 144 h for morulae
formation. Diazinon did not affect oocyte viability and embryo divisions but decreased IVF (fertilization inhibition 50 = 502 μM) and morulae formation (morulae inhibition 50 = 344 μM). Malathion affected all the studied parameters: lethal concentration 50 = 1 mM, fertilization inhibition 50 = 443 μM, development inhibition 50 = 375 μM, and morulae inhibition 50 = 216 μM. The results of this study indicate that diazinon and malathion used in commercial formulation could be toxic, producing
impairment in in vitro fertilization and embryo development. This is an approach for further investigations to find out cell
damage mechanisms produced by these widely used insecticides. 相似文献
11.
Until now, physiological mechanisms and downstream targets responsible for the cadmium (Cd) tolerance mediated by endogenous hydrogen sulfide (H 2S) have been elusive. To address this gap, a combination of pharmacological, histochemical, biochemical and molecular approaches was applied. The perturbation of reduced (homo)glutathione homeostasis and increased H 2S production as well as the activation of two H 2S-synthetic enzymes activities, including L-cysteine desulfhydrase (LCD) and D-cysteine desulfhydrase (DCD), in alfalfa seedling roots were early responses to the exposure of Cd. The application of H 2S donor sodium hydrosulfide (NaHS), not only mimicked intracellular H 2S production triggered by Cd, but also alleviated Cd toxicity in a H 2S-dependent fashion. By contrast, the inhibition of H 2S production caused by the application of its synthetic inhibitor blocked NaHS-induced Cd tolerance, and destroyed reduced (homo)glutathione and reactive oxygen species (ROS) homeostases. Above mentioned inhibitory responses were further rescued by exogenously applied glutathione (GSH). Meanwhile, NaHS responses were sensitive to a (homo)glutathione synthetic inhibitor, but reversed by the cotreatment with GSH. The possible involvement of cyclic AMP (cAMP) signaling in NaHS responses was also suggested. In summary, LCD/DCD-mediated H 2S might be an important signaling molecule in the enhancement of Cd toxicity in alfalfa seedlings mainly by governing reduced (homo)glutathione and ROS homeostases. 相似文献
12.
Hydrogen sulfide (H 2S) is a gaseous messenger and serves as an important neuromodulator in the central nervous system. The current study was undertaken
to investigate whether H 2S attenuates the neuronal injury induced by vascular dementia (VD). Rats were subjected to bilateral common carotid artery
and vertebral artery occlusion for 5 min three times in an interval of 5 min to induce VD. An H 2S donor, sodium hydrosulfide (NaHS) or an inhibitor of cystathionine-β-synthase, hydroxylamine (HA) was administered intraperitoneally.
The number of neurons in the hippocampus was determined by hematoxylin and eosin staining, and the performance of learning
and memory was tested by the Morris water maze. H 2S content in plasma was evaluated. Apoptosis in the hippocampus was assessed by flow cytometry. In addition, Bcl-2 and Bax
expression was analyzed by immunohistochemical staining. The neuronal injury occurred gradually with a decreased number of
neurons and increased apoptosis ratio in the hippocampus over 720 h after VD. The H 2S level was also gradually decreased in plasma over 720 h after VD, which negatively correlated with the apoptosis ratio in
the hippocampus after VD. In addition, NaHS treatment significantly attenuated neuronal injury and improved neural functional
performance, whereas HA exaggerated the neuronal injury and exacerbated learning and memory at 720 h after VD. Furthermore,
NaHS treatment markedly improved the ratio of Bcl-2 over Bax with increased Bcl-2 expression and decreased Bax expression.
In contrast, HA reduced the ratio of Bcl-2 over Bax. It is suggested that H 2S attenuates VD injury via inhibiting apoptosis and may have potential therapeutic value for VD. 相似文献
13.
In vitro and in vivo studies have proven strontium to be an osteoinductive trace element. The effect of strontium ranelate
(SR) on H 2O 2-induced apoptosis of CRL-11372 cells and optimization of its anti-apoptotic dose were the aims of this study. After 1 h of
pretreatment with SR 1 μM, 50 μM, 100 μM, 500 μM, and 1,000 μM concentrations, CRL-11372 osteoblasts were exposed to 100 μM H 2O 2 for periods of 6–12 h. The same experiments were repeated without H 2O 2. The apoptotic index and viability of cells were assessed quantitatively with a fluorescent dye and qualitatively with agarose
gel electrophoresis. Concentrations of 1–100 μM of SR with a 6-h treatment and only 1 μM concentration with a 12-h treatment
inhibited the apoptotic effect of H 2O 2 on cultured osteoblasts significantly ( P < 0.05). SR was shown to inhibit H 2O 2-induced apoptosis of CRL-11372 cells in a dose-dependent manner. 相似文献
14.
The mechanism of action of Hydrogen sulfide (H 2S) as a novel endogenous gaseous messenger and potential cardioprotectant is not fully understood. We therefore investigated the prevention of cardiomyocyte apoptosis by exogenous H 2S and the signaling pathways leading to cardioprotection. Using a simulated ischemia–reperfusion (I/Re) model with primary cultured rat neonatal cardiomyocytes, I/Re induced a rapid, time-dependent phosphorylation of c-Jun N-terminal kinase (JNK), with significant elevation at 0.25 h and a peak at 0.5 h during reperfusion. NaHS (H 2S donor) significantly inhibited the early phosphorylation of JNK, especially at 0.5 h. Both NaHS and SP600125 (specific JNK inhibitor) decreased the number of apoptotic cells, lowered cytochrome C release and enhanced Bcl-2 expression. When NaHS application was delayed 1 h after reperfusion, the inhibition of apoptosis by H 2S was negated. In conclusion, this is novel evidence that early JNK inhibition during reperfusion is associated with H 2S-mediated protection against cardiomyocyte apoptosis. 相似文献
15.
以黑籽南瓜(Cucurbita ficifolia)种子为试材, 研究了外施不同浓度的NaHS对NaHCO 3胁迫下种子萌发及生理特性的影响。结果表明, NaHCO 3胁迫显著抑制了黑籽南瓜种子的发芽率、胚轴长和胚根长, 降低了种子萌发过程中的可溶性糖含量, 抑制了α-淀粉酶、β-淀粉酶、SOD及POD活性。而外施不同浓度的NaHS显著促进了NaHCO 3胁迫下黑籽南瓜萌发种子胚轴和胚根的生长, 提高了可溶性糖含量及α-淀粉酶、β-淀粉酶、SOD和POD活性, 降低了MDA含量; 外施其它盐类(Na 2S、Na 2SO4、NaHSO 4和NaHSO 3)及不同pH值(pH5.8–7.8)的Na 2HPO 4-NaH 2PO 4缓冲液对NaHCO 3胁迫下黑籽南瓜种子的萌发则无影响。外施NaHS可有效缓解NaHCO 3胁迫对黑籽南瓜种子萌发的抑制作用, 其缓解效应可能与其释放的H 2S有关。 相似文献
16.
Hydrogen sulfide (H2S) is now considered to be a gasotransmitter and may be involved in the pathological process of Alzheimer’s disease (AD). A majority of APP is associated with mitochondria and is a substrate for the mitochondrial γ-secretase. The mitochondria-associated APP metabolism where APP intracellular domains (AICD) and Aβ are generated locally and may contribute to mitochondrial dysfunction in AD. Here, we aimed to investigate the ability of H2S to mediate APP processing in mitochondria and assessed the possible mechanisms underlying H2S-mediated AD development. We treated neurons from APP/PS1 transgenic mice with a range of sodium hydrosulfide (NaHS) concentrations. NaHS attenuated APP processing and decreased Aβ production in mitochondria. Meanwhile, NaHS did not changed BACE-1 and ADAM10 (a disintegrin and metalloprotease 10) protein levels, but NaHS (30 μM) significantly increased the levels of presenilin 1(PS1), PEN-2, and NCT, as well as improved the γ-secretase activity, while NaHS (50 μM) exhibits the opposing effects. Furthermore, the intracellular ATP and the COX IV activity of APP/PS1 neurons were increased after 30 μM NaHS treatment, while the ROS level was decreased and the MMP was stabilized. The effect of NaHS differs from DAPT (a non-selective γ-secretase inhibitor), and it selectively inhibited γ-secretase in vitro, without interacting with Notch and modulating its cleavage. The results indicated that NaHS decreases Aβ accumulation in mitochondria by selectively inhibiting γ-secretase. Thus, we provide a mechanistic view of NaHS is a potential anti-AD drug candidate and it may decrease Aβ deposition in mitochondria by selectively inhibiting γ-secretase activity and therefore protecting the mitochondrial function during AD conditions. 相似文献
17.
ObjectivesThis study examined the dose-dependent actions of hydrogen sulfide donor sodium hydrosulphide (NaHS) on isometric contractions and ion transport in rat aorta smooth muscle cells (SMC). MethodsIsometric contraction was measured in ring aortas segments from male Wistar rats. Activity of Na +/K +-pump and Na +,K +,2Cl -cotransport was measured in cultured endothelial and smooth muscle cells from the rat aorta as ouabain-sensitive and ouabain-resistant, bumetanide-sensitive components of the 86Rb influx, respectively. ResultsNaHS exhibited the bimodal action on contractions triggered by modest depolarization ([K +] o=30 mM). At 10 ?4 M, NaHS augmented contractions of intact and endothelium-denuded strips by ~ 15% and 25%, respectively, whereas at concentration of 10 ?3 M it decreased contractile responses by more than two-fold. Contractions evoked by 10 ?4 M NaHS were completely abolished by bumetanide, a potent inhibitor of Na +,K +,2Cl -cotransport, whereas the inhibition seen at 10 ?3 M NaHS was suppressed in the presence of K + channel blocker TEA. In cultured SMC, 5×10 ?5 M NaHS increased Na +,K +,2Cl - - cotransport without any effect on the activity of this carrier in endothelial cells. In depolarized SMC, 45Ca influx was enhanced in the presence of 10 ?4 M NaHS and suppressed under elevation of [NaHS] up to 10 ?3 M. 45Ca influx triggered by 10 ?4 M NaHS was abolished by bumetanide and L-type Ca 2+ channel blocker nicardipine. ConclusionsOur results strongly suggest that contractions of rat aortic rings triggered by low doses of NaHS are mediated by activation of Na +,K +,2Cl -cotransport and Ca 2+ influx via L-type channels. 相似文献
18.
Previous studies have shown that the in ovo injection of equol can markedly improve the water-holding capacity of muscles
of broilers chickens at 7 wk of age through promotion of the antioxidant status. We aimed to investigate directly the antioxidant
effects of equol on muscle cells in broilers. Muscle cells were separated from leg muscle of embryos on the 11th day of incubation
and treated with equol and H 2O 2, either alone or together. Cells were pretreated with medium containing 1, 10, or 100 μM equol for 1 h prior to the addition
of 1 mM H 2O 2 for a further 1 h. Photomicrographs of cells were obtained. Cell viability, malondialdehyde (MDA) content, and L-lactate
dehydrogenase (LDH) activity in the cell supernatant, as well as intracellular total superoxide dismutase (T-SOD) and glutathione
peroxidase (GSH-Px) activities were determined. Treatment with 1 mM H 2O 2 caused serious damage to cells, indicated by comets with no clear head region but a very apparent tail of DNA fragments.
Pretreatment with low (1 μM) but not high concentrations of equol (10 μM) inhibited cell damage, while 100 μM equol caused
more serious damage than H 2O 2 alone. Pretreatment with 1 μM equol had no effect on cell viability, while pretreatment with 10 and 100 μM equol significantly
decreased cell viability in a dose-dependent manner. Compared with H 2O 2 alone, pretreatment with low-dosage equol markedly decreased LDH activity and MDA production in the supernatant, significantly
increased intracellular T-SOD activity ( P < 0.05) and tended to increase intracellular GSH-Px activity (0.05 < P < 0.1). Pretreatment with high-dosage equol (10 and 100 μM) significantly enhanced LDH activity, but had no effect on MDA
content, T-SOD or GSH-Px activity induced by H 2O 2, except for an obvious increase in GSH-Px activity caused by 10 μM equol. These results indicate that equol at low dosage
can prevent skeletal muscle cell damage induced by H 2O 2, while pretreatment with high-dosage equol shows a synergistic effect with H 2O 2 in inducing cell damage. 相似文献
19.
To improve the nutritional value of chickpea food, selenium (Se)-rich chickpea sprouts were produced by germination of chickpea
seeds for 6 days at 28 centigrade in the presence of various concentrations of Na 2SeO 3 in germination solution. High concentrations of selenite were found to inhibit the growth of chickpea sprout and the biosynthesis
of isoflavones formononetin and biochanin A. However, chickpea sprouts could tolerate up to ∼50 mg/L of Na 2SeO 3, under which condition the product chickpea sprouts contained a high Se content (2.14 μg/g dry weight) and a moderate high
content of isoflavones (601.56 μg biochanin A/g dry weight and 578.11 μg formononetin/g dry weight). Se was incorporated in
chickpea sprout in the form of selenomethionine. Thus, Se-enriched chickpea sprouts may serve as a convenient dietary source
of Se and of isoflavones, including formononetin and biochanin A. 相似文献
20.
Dietary chromium(III) picolinate (CrPic) effects on circulating steroid hormones have been reported in various experimental
animals. However, direct effects of CrPic on adrenocortical steroidogenesis are uncertain. Therefore, the objective was to
determine the effects of CrPic on cortisol and dehydroepiandrosterone sulfate (DHEAs) secretion from H295R cells. In experiment
1, a 24-h exposure to CrPic (0 to 200 μM) had both linear ( p < 0.001) and quadratic ( p < 0.001) effects on cortisol secretion from forskolin-stimulated cells with the highest cortisol secretion at 0.1 μM of CrPic
and the lowest at 200 μM of CrPic. In experiment 2, a 48-h exposure to CrPic (200 μM) decreased cortisol ( p < 0.07) release from forskolin-stimulated cells during a 24-h collection period. In experiment 3, a 48-h exposure to CrPic
(100 μM) decreased cortisol ( p < 0.05) and DHEAs ( p < 0.01) from forskolin-stimulated cells during a 24-h sampling period. In experiment 4, a 24-h exposure to forskolin followed
by a 24-h exposure to both forskolin and CrPic (100 and 200 μM) decreased both cortisol and DHEAs secretion ( p < 0.01). This study suggests that at high concentrations, CrPic inhibits aspects of steroidogenesis in agonist-stimulated
adrenocortical cells. 相似文献
|