Sulfur Dioxide Derivatives Research Articles

Vasodilatation of sulfur dioxide derivatives and signal transduction

The vasodilatation of sulfur dioxide (SO 2) derivatives on the rat thoracic aortic rings and its cell signal transduction pathway were studied. The levels of cAMP, cGMP, PGI 2, TXA 2 and activities of PKA and adenylyl cyclase (AC) in the rings exposed to SO 2 derivatives were determined. The results indicated that SO 2 derivatives could dose-dependently relax the isolated rat aorta rings with or without endothelium precontracted by NE, no difference was found between the rings with and without endothelium; Levels of cAMP, PGI 2, AC activity and PKA activity in the aortic rings were significantly increased by the derivatives in a dose-related way; No change of cGMP and TXA 2 levels in rings was observed; cAMP/cGMP and PGI 2/TXA 2 ratios were increased significantly by the SO 2 derivatives. These results led to the conclusions that SO 2 derivatives might cause the endothelium-independent vasorelaxation effect, and the vasorelaxation was mediated in partly by the signal transduction pathway of PGI 2-AC-cAMP-PKA.

Sulfur dioxide derivatives modulate Na/Ca exchange currents and cytosolic [Ca 2+] i in rat myocytes

We have recently shown that sulfur dioxide (SO 2) derivatives (bisulfite and sulfite, 1:3 M/M) modulated L-type calcium, sodium, and potassium channels in rat myocytes. The aim of this study was to investigate whether SO 2 derivatives could alter Na/Ca exchanger current and the intracellular free [Ca 2+]. The nickel-sensitive Na/Ca exchanger current was measured in rat myocytes exposed to ramp pulses in Tyrode’s solution containing ouabain, nifedipine, and ±Ni (5 mmol/l). Myocytes were loaded with the fluorescent Ca 2+ indicator Fura-2/AM to estimate intracellular Ca 2+ concentration. SO 2 derivatives significantly inhibited both outward and inward Ni-sensitive Na/Ca exchanger currents without a shift in the reversal potential. The intracellular free [Ca 2+] was raised by SO 2 derivatives in several concentrations. SO 2 derivatives increased [Ca 2+] i in rat myocytes and its mechanism might involve SO 2 derivatives significantly inhibiting Na/Ca exchanger current and enhancing L-type calcium channel.

The Vasodilator Effect and Its Mechanism of Sulfur Dioxide-Derivatives on Isolated Aortic Rings of Rats

The vasodilator effect of exogenous sulfur dioxide (SO2) derivatives (mixture of sodium bisulfite and sodium sulfite, 3:1 M/M in neutral solution) on rat vascular system was studied in order to explore the mechanism of blood pressure lowered by SO2 and its derivatives. Isolated rat aortic rings were perfused in bath tubes containing various chemicals and their tensions were recorded. The results showed: (1) The SO2 derivatives could relax isolated aorta precontracted by norepinephrine (NE) or potassium chloride (KCl) in a dose-dependent manner. (2) This vasodilator effect was attenuated after preincubation with indomethacin, but was not affected by N-L-nitro-arginine, methylene blue, and propranolol, and was independent of the aorta endothelium. (3) The vasoconstriction responses induced by NE, KCl, or Ca2+ were antagonized by SO2 derivatives in a noncompetitive manner. (4) The vasoconstrictions of two components (initial fast vasoconstriction induced by intracellular Ca2+ release and sustained vasoconstriction evoked by extracellular Ca2+ influx) were also inhibited by SO2 derivatives. These results led to the conclusions: The SO2 derivatives could cause vasorelaxation by a direct role of the chemicals on aortic smooth muscle cells. It was not dependent on vascular endothelium and was independent of nitric oxide (NO). It is suggested that SO2 and its derivatives might be also vasoactive substances that modulate changes of blood pressure, like other gasotransmitters. The vasorelaxation might be related to the inhibition effects of SO2 derivatives on Ca2+ entry through both potential-dependent calcium channels and receptor-operating calcium channels, and also to the inhibition of intracellular Ca2+ release. The vasorelaxation was at partly related to the increase of prostacyclin (PGI2) induced by SO2 derivatives.

Sulfur dioxide derivatives modulation of high-threshold calcium currents in rat dorsal root ganglion neurons

This study addressed the effect of sulfur dioxide (SO 2) derivatives on high-voltage-activated calcium currents (HVA- I Ca) in somatic membrane of freshly isolated rat dorsal root ganglion (DRG) neurons by using the whole-cell configuration of patch-clamp technique. High-threshold Ca 2+ channels are highly expressed in small dorsal root ganglion neurons. SO 2 derivatives increased the amplitudes of calcium currents in a concentration-dependent and voltage-dependent manner. The 50% enhancement concentrations (EC 50) of SO 2 derivatives on HVA- I Ca was about 0.4 μM. In addition, SO 2 derivatives significantly shifted the activation and inactivation curve in the depolarizing direction. Parameters for the fit of a Boltzmann equation to mean values for the activation were V 1/2 = −17.9 ± 1.3 mV before and −12.5 ± 1.1 mV after application 0.5 μM SO 2 derivatives 2 min ( P < 0.05). The half inactivation of HVA- I Ca was shifted 9.7 mV to positive direction ( P < 0.05). Furthermore, SO 2 derivatives significantly prolonged the slow constant of inactivation, slowed the fast recovery but markedly accelerated the slow recovery of HVA- I Ca from inactivation. From HP of −60 mV 0.5 μM SO 2 derivatives increased the amplitude of HVA- I Ca with a depolarizing voltage step to −10 mV about 54.0% in small DRG neurons but 33.3% in large DRG neurons. These results indicated a possible correlation between the change of calcium channels and SO 2 inhalation toxicity, which might cause periphery neurons abnormal regulation of nociceptive transmission via calcium channels.

Study of the interaction of sulfur dioxide derivative with cardiac sodium channel

The effects of sulfur dioxide (SO 2) derivatives (bisulfite and sulfite, 1:3 M/M) on voltage-dependent sodium channel in isolated rat ventricular myocyte were studied using the whole cell patch-clamp technique. SO 2 derivatives increased sodium current ( I Na) in a concentration-dependent manner. SO 2 derivatives at 10 μM significantly shifted steady-state inactivation curve of I Na to more positive potentials, but did not affect the activation curve. SO 2 derivatives markedly shifted the curve of time-dependent recovery of I Na from inactivation to the left, and accelerated the recovery of I Na. SO 2 derivatives also significantly shortened the activation and inactivation time constants of I Na. These results indicated that SO 2 derivatives produced concentration-dependent stimulation of cardiac sodium channels, which due mainly to the interaction of the drug with sodium channels in the inactivated state.

Modulation of L-type calcium current in rat cardiac myocytes by sulfur dioxide derivatives

The effects of sulfur dioxide (SO 2) derivatives (bisulfite and sulfite, 1:3 M/M) on voltage-dependent L-type calcium current ( I Ca,L) in isolated rat ventricular myocytes were studied using the whole cell patch-clamp technique. SO 2 derivatives increased I Ca,L in a concentration-dependent manner. SO 2 derivatives shifted both the steady-state activation and the inactivation curves of I Ca,L to more positive potentials, the effect on the latter being more pronounced. SO 2 derivatives markedly accelerated the recovery of I Ca,L from inactivation. SO 2 derivatives also significantly shortened the fast and slow time constants of inactivation. These results suggested that SO 2 inhalation might cause cardiac myocyte injury through increasing intracellular calcium via voltage-gated calcium channels.

Sulfur dioxide derivative modulation of potassium channels in rat ventricular myocytes

The effects of sulfur dioxide (SO 2) derivatives (bisulfite and sulfite, 1:3 M/M) on voltage-dependent potassium current in isolated adult rat ventricular myocyte were investigated using the whole cell patch–clamp technique. SO 2 derivatives (10 μM) increased transient outward potassium current ( I to) and inward rectifier potassium current ( I K1), but did not affect the steady-state outward potassium current ( I ss). SO 2 derivatives significantly shifted the steady-state activation curve of I to toward the more negative potential at the V h point, but shifted the inactivation curve to more positive potential. SO 2 derivatives markedly shifted the curve of time-dependent recovery of I to from the steady-state inactivation to the left, and accelerated the recovery of I to from inactivation. In addition, SO 2 derivatives also significantly change the inactivation time constants of I to with increasing fast time constant and decreasing slow time constant. These results indicated a possible correlation between the change of properties of potassium channel and SO 2 inhalation toxicity, which might cause cardiac myocyte injury through increasing extracellular potassium via voltage-gated potassium channels.

DNA damaging effects of sulfur dioxide derivatives in cells from various organs of mice

The DNA-damaging effects of sulfur dioxide (SO2) derivatives (a mixture of sodium sulfite and sodium bisulfite, 3:1 M/M) in the cells of various organs (brain, lung, heart, liver, stomach, spleen, thymus, bone marrow and kidney) of male mice were studied using the single cell gel electrophoresis technique (SCGE). Three groups of six mice each received an i.p. dose of SO2 derivatives (125, 250 or 500 mg/kg body wt) daily for 7 days. A control group of six mice received 200 microl of normal saline i.p. daily for 7 days. Our results show that SO2 derivatives caused significant increases in olive tail moment (OTM) in cells from all organs tested in a dose-dependent manner. These results show that SO2 derivatives can cause DNA damage to multiple organs of mice and that SO2 derivatives are systemic DNA-damaging agents, not only to the respiratory system. It is suggested that SO2 derivative exposure has a potential risk to DNA in multiple organs of mammals and might be related to carcinogenesis or other diseases related to DNA damage. Further work is required to understand the toxicological role of SO2 and its derivatives on multiple or even all organs in humans and animals. Recent research results have shown that SO2 and its derivatives can also induce an increase in the frequencies of chromosomal aberrations, sister chromatid exchanges and micronuclei in mammalian cells and cause oxidative damage in multiple organs of male and female mice. Taken together, these results suggest that SO2 and its derivatives are systemic toxic agents. However, further studies need to be performed before a definitive conclusion can be drawn.

Modulation of sodium currents in rat dorsal root ganglion neurons by sulfur dioxide derivatives

The effect of sulfur dioxide (SO 2) derivatives, a common air pollutant and exists in vivo as an equilibrium between bisulfate and sulfite, on tetrodotoxin-sensitive (TTX-S) and tetrodotoxin-resistant (TTX-R) sodium channels in cultured post-natal dorsal root ganglion (DRG) neurons were studied using the whole cell configuration of patch-clamp technique. SO 2 derivatives on two types of sodium currents were either inhibitory or stimulatory depending on the kinetic parameters tested. At a holding potential of −80 mV, SO 2 derivatives suppressed TTX-S sodium currents when depolarizing potential was negative to −30 mV and TTX-R sodium currents when negative to −10 mV but they increased them when the depolarizing potential was positive to −30 or −10 mV. SO 2 derivatives shifted the conductance–voltage curve for TTX-R sodium currents in the depolarizing direction but had little effect on that for TTX-S sodium currents. The steady-state inactivation curve for TTX-R sodium channel was shifted by SO 2 derivatives in the depolarizing direction as that for TTX-S sodium channel. SO 2 derivatives changed the reversal potential and increased the maximum conductance of two types of sodium channels. SO 2 derivatives postponed the activating time and delayed the inactivation of sodium currents. The results suggest that SO 2 derivatives would increase the excitability of neurons and alter the ion selectivity for two types of sodium currents.

ChemInform Abstract: RAMAN STUDY OF COMPLEXES BETWEEN SULFUR DIOXIDE AND SOME PYRIDINE DERIVATIVES

Chemischer InformationsdienstVolume 13, Issue 8 Physical Organic Chemistry ChemInform Abstract: RAMAN STUDY OF COMPLEXES BETWEEN SULFUR DIOXIDE AND SOME PYRIDINE DERIVATIVES Z. PAWELKA, Z. PAWELKASearch for more papers by this authorG. MAES, G. MAESSearch for more papers by this authorTH. ZEEGERS-HUYSKENS, TH. ZEEGERS-HUYSKENSSearch for more papers by this author Z. PAWELKA, Z. PAWELKASearch for more papers by this authorG. MAES, G. MAESSearch for more papers by this authorTH. ZEEGERS-HUYSKENS, TH. ZEEGERS-HUYSKENSSearch for more papers by this author First published: February 23, 1982 https://doi.org/10.1002/chin.198208052AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume13, Issue8February 23, 1982 RelatedInformation