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<p><b>OBJECTIVE</b>To investigate the induction effects of sulfur dioxide (SO(2)) inhalation on chromosomal aberrations (CA) in mouse bone marrow cells.</p><p><b>METHODS</b>The mice were treated with SO(2) for 4 h/day x 7 days at various concentrations of SO(2), then mitotic indices and CA in the bone marrow cells were analyzed.</p><p><b>RESULTS</b>SO(2) increase the frequencies of CA and aberrant cells in mouse bone marrow cells in dose-dependent manner. The frequencies (%) of the aberrant cells in mouse bone marrow cells induced by SO(2) at concentrations of 0, 14, 28, 56 and 84 mg/m(3) were 1.81, 3.00, 3.58, 4.26 and 4.86, respectively. SO(2) at low concentrations induced only chromatid-type CA, but at high concentrations it induced both chromatid-type and chromosome-type CA. SO(2) inhalation decreased the mitotic indices of the bone marrow cells.</p><p><b>CONCLUSIONS</b>SO(2) inhalation may inhibit mitoses and increase CA frequencies of the bone marrow cells; therefore, it is a clastogenetic and genotoxic agent. It implies that long time exposure of SO(2) pollutant at low concentration in air may be a potential risk to induce damage of cytogenetic material in humans.</p>
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Animals , Female , Male , Mice , Administration, Inhalation , Bone Marrow Cells , Metabolism , Pathology , Chromosome Aberrations , Dose-Response Relationship, Drug , Mitotic Index , Sulfur Dioxide , PharmacologyABSTRACT
<p><b>OBJECTIVE</b>To investigate the inhalation of sulfur dioxide (SO(2)) on the DNA damage of brain cells in mammalian animals.</p><p><b>METHOD</b>Single cell microgel electrophoresis technique (comet test) was used to test the DNA damage of brain cells.</p><p><b>RESULTS</b>(1) After the exposure to SO(2) at 0, 7, 14, 28 mg/m(3), the tail lengths of nuclear DNA in brain cells from male mice were 8.02, 23.14, 46.43 and 53.49 micro m respectively; and that from female mice were 7.23, 12.43, 20.39 and 54.83 micro m respectively. The results showed that: (1) SO(2) inhalation caused damage on DNA of brain cells in a dose-dependent manner; (2) Even under lower concentration of SO(2) as 7 mg SO(2)/m(3), the damage on DNA of brain cells was also reached to 98.8%. It implied that the brain cells of mammalian animals were very sensitive to SO(2) inhalation; (3) The DNA damage of brain cells from male mice is more serious than that from female mice. The reasons remain to be further studied.</p><p><b>CONCLUSIONS</b>SO(2) pollution even at lower concentrations also had a potential risk to the genetic material DNA of brain cells from mammalian animals. The results of our study might explain the recently published epidemiological studies that the workers exposed to SO(2) or SO(2) derivatives had suffered an increase of mortality from brain cancer.</p>
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Animals , Female , Male , Mice , Administration, Inhalation , Brain , Metabolism , DNA , DNA Damage , Dose-Response Relationship, Drug , Sulfur Dioxide , ToxicityABSTRACT
AIM: To study the effects of sodium metabisulfite (SMB), sulfur dioxide (SO_2) and its derivatives in vivo, sodium bisulfite and sulfite, on Na~+ currents. The effects of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) against SMB were also studied in freshly dissociated hippocampal CA1 neurons in rats. METHODS: The whole-cell patch-clamp techniques were used in the experiments. RESULTS: ① SMB increased the voltage-activated Na~+ currents in a concentration-and voltage-dependent manner. The amplitudes of Na~+ currents was increased (22.36?3.28) % and (65.05?5.75)% (n=10) by SMB at 2 ?mol/L and 20 ?mol/L, respectively. ② SMB (10 ?mol/L) did not affect the activation process, but changed the inactivation process significantly. Before and after application of 10 ?mol/L SMB, the half-inactivation voltage was (-82.38)?0.54) mV and (-69.39)?0.41) mV (n=10, P
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The developments of domestic and foreign researches on mutagenesis of sulfur dioxide were briefly reviewed in this paper from different aspects: microbiological experiments, the experiments of cultured mammalian cells in vitro,experiments on mammal and population in vivo.
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Objective The aims of the present study are to further investigate mechanism of toxicological role of sulfur dioxide (SO 2) exposure on mammalian animals Methods Effects of SO 2 inhalation (14 mg/m 3) on activities of antioxidative enzymes and levels of lipid peroxidation in erythrocytes of male rats were determined Results SO 2 inhalation caused the decrease of Cu,Zn SOD activity,the increase of GSH Px activity,and no change of CAT activity,and the increase of level of lipid peroxidation in rat erythrocytes Conclusion Primary mechanism of toxicological role of SO 2 exposure at low concentrations may be that oxidation damages of lipid and other biological large moleculars are caused by SO 2 producing reactive oxygen species
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Objective To study the effects of sulphur dioxide(SO 2 )inhalation on the blood pressure of rats.Methods The male Wistar rats were exposed to28.6,57.3and114.4mg /m 3 SO 2 six hours each day for7days respectively by the tech-nique of dynamic fumigation and the ratsblood pressures were measured using RBP-1model blood pressure meter every day af-ter the SO 2 inhalation.Results28.6mg /m 3 SO 2 inhalation could cause a decrease of the ratsblood pressures compared with the background value at3rd and4th day(P
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Objective To study lexicological effects of sulfur dioxide (SO2) on reproductive system of male mammals. Methods After dynamic 7-day inhalation of SO2 at various concentrations, such as (22
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Whether three genes [?-aminolevulinic acid dehydratase (ALAD) gene, Vitamin D receptor (VDR) gene and hemochromatosis gene] can make certain individuals more vulnerable to lead are discussed. Polymorphisms of ALAD gene have been associated with the accumulation and distribution of lead in the blood, bone and internal organs in humans and animals. VDR gene has been implicated in the control of calcitriol levels in serum, which normally regulates calcium absorption and can in turn affect lead levels. Hemochromatosis gene, associated with a disease that leads to excessive iron accumulation, may also influence the absorption of lead.
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Objective To study the mechanism of rat blood pressure lowered by SO2 and SO2 derivatives.Methods 6-Keto-PGF1? and TXB2 were determined by radioimmunoassay in the plasma and aorta tissue of rats.Results The 6-Keto increased significantly in the isolated aortic rings in all exposure groups except 8 mmol/L group.No change of TXB2 was observed in the rings in all exposure groups.Meanwhile,6-Keto/TXB2 ratios increased significantly at 2 mmol/L and 4 mmol/L.Compared with the control group,6-Keto level decreased significantly in the plasma of the rats exposed to SO2 at 14 mg/m3,28mg/m3 and 56 mg/m3,but the level of TXB2 increased significantly.6-Keto/TXB2 ratios decreased gradually with the increase of SO2 concentration.Conclusion PGI2 and TXA2 are possibly changed by SO2 and SO2 derivatives,which regulates partly rat blood pressure.
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Objective To study the distribution of the sulfur dioxide (SO2) in the different organs of mice after exposed to SO2. Methods The Kunming mice were exposed to SO2 at different doses in a chamber in which the concentration of SO2 could be monitored. The concentrations of sulfite in livers, kidneys, spleens and testis from male mice were determined by high performance liquid chromatography (HPLC) with fluorescence detection (FD). After reduction, pre-column derivation to tissue homogenates of livers, kidneys, spleens and testis, the mixture was centrifuged, and 5 ?l of the resulting supernatant was directly injected into HPLC with analytical column C18(200 mm ? 5.0 mm, 5 ?m), where the mobile phase consisted of a mixture methanol-water(contained 0.25% acetic acid ) (10:90,V/V), pH was 2.8 adjusted with phosphoric acid, and the exciting and emitting wavelength of fluorescence detection were 392nm and 479nm,respectively. The mobile phase was pumped at a flow rate of 1.0 ml/min, and the column temperature was 30 ℃. Results The standard curve of sulfite was linear in the range from 0.063 ?g/ml to 1.26 ?g/ml (r=0.997 8), and the minimal detectable concentration was 0.05 ?g/ml (S/N=3) with a recovery rates of 95%-101%. The relative standard deviations (RSD) of intra-day and inter-day RSD were less than 10%. The results showed that sulfite concentration in all organs tested from mice in SO2-exposed groups was significantly increased (P
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Objective To investigate the genetic damage of dust storm fine particles on human blood lymphocytes. Methods The chromosomal aberration test and cytochalasin B blocked test were used to investigate the effect in vitro of dust storm fine particles (PM2.5) (0, 33, 100, 300 ?g/ml)collected in Baotou and Wuwei cities on human lymphocytes. Results In both dust storm and normal ambient air fine particles treated cells revealed an increase in the chromosomal aberration level and micronuclei frequency (MNF). The chromosomal aberration(CA)were characterized as chromatid break, chromosome break, acentric fragment, dicentric chromosome and gaps. With the increase of treatment concentrations the aberration level and MNF increased and the mitotic index(MI) and the nuclear division index (NDI) values declined in a dose-response manner(P0.05). The treatments of normal ambient air PM2.5 from Baotou City were significant higher than those of Wuwei City, but the treatments of dust storm PM2.5 were not significant different between the cities. Conclusion Dust storm PM2.5 from Baotou City and Wuwei City may cause human lymphocytes genetic damage and its genetic toxicity is related to the dose.
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Objective To investigate the effects of airborne fine particulate matter(PM2.5) on anti-oxidative enzymes activities and lipid peroxidation levels in livers, spleens, and kidneys of rats. Methods 32 male Wistar rats were randomly divided into PM2.5 exposure groups of different concentration (1.5, 7.5, 37.5 mg/kg), exposed by tracheoperfusion and control group treated with physiological saline. Rats were killed 24 h after treatment, and the levels of thiobarbituric acid reactive substance (TBARS), glutathione(GSH) and activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) were determined. Results PM2.5 exposure caused significantly decrease of SOD, CAT, GSH-Px, SOD/TBARS in livers and kidneys in a dose-dependent manner compared with control group (P
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AIM and METHODS: The effects of hydrogen peroxide on Na+ currents were studied in freshly dissociated rat hippocampal CA1 neurons using the whole-cell patch-clamp techinique. RESULTS: 2貶 2O 2 caused a dose-dependent and voltage-dependent increase in the voltage-activated Na+ currents. The amplitudes of Na+ currents were increased (48.0?4.2)% and (88. 2?5. 1)% (n=10) by H 2O 2 at 10 ?mol/L and 100 ?mol/L, respectively. ②H 2O 2 (10 ?mol/L) did not affect the activation process, but changed the inactivation process significantly. Before and after application of 10 ?mol/L of H 2O 2, the half-inactivation voltage was (-64.58?1.22)mV and (-53.55?0.94)mV (n=10, P
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AIM:To probe into the toxicological mechanism of sulfur dioxide (SO2) and its derivatives on cardiovascular system.METHODS: Effects of tea polyphenols (TP) on the increase in sodium current (INa) induced by SO2 derivatives in the cardiomyocytes were studied using the whole cell patch-clamp technique.RESULTS: ① The increase in INa induced by SO2 derivatives was inhibited by treating the cells with TP at different concentrations (10, 20 or 50 mg/L) in a dose dependent manner. At concentration of 50 mg/L, TP completely inhibited the increase in INa by SO2 derivatives. ② SO2 derivatives led to shift left of the activation curve. After application of TP at dose of 50 mg/L, the curve showed resumed significantly. ③ TP changed the inactivation process significantly. Before and after the application of SO2 derivatives, the half-inactivation voltage of INa was -(71.94?0.23) mV and -(65.79?0.69) mV (n=8, P0.05).CONCLUSION: TP inhibits the incremental effects of SO2 derivatives on INa, suggesting that the toxicity of SO2 on cardiomyocytes of rat is induced by free radical.