接触二硫化碳大鼠铜水平与血浆LCAT活性的变化及关系的研究

ＳＤ大鼠分别用５ｍｇ／ｍ３和５０ｍｇ／ｍ３ＣＳ２吸入染毒６个月。结果表明：５０ｍｇ／ｍ３ＣＳ２接触组肝铜含量显著减少（Ｐ＜０．０５），血浆ＬＣＡＴ活性显著抑制（Ｐ＜０．０１）。肝铜含量与血浆ＬＣＡＴ活性呈正线性相关（Ｐ＜０．０１）。实验结果提示：ＣＳ２能引起铜代谢紊乱，降低体内铜水平；血浆ＬＣＡＴ是一种铜酶；ＣＳ２可通过干扰铜代谢，从而抑制ＬＣＡＴ活性，引起脂质代谢紊乱。     

职业接触低浓度二硫化碳对血胆固醇及冠心病患病率影响的调查

目的 研究职业接触低于阈限值一时间加权平均值(TLV-TWA)(31mg/m^3)的二硫化碳(CS2)对血总胆固醇、冠心病患病率的影响。方法①采用WHO标准化的调查表询问调查对象的医学史和工作史；②统一组织被调查者到正规医院做12导联心电图检查；③统一采集被调查者早晨空腹静脉血测定总胆固醇。④用SPSS7．5软件进行统计分析。结果接触组CS2指数＞100组与对照组血总胆固醇差异有非常显著性(t=3．49，P＜0．01)，但两组冠心病患病率无明显差别。结论 接触低浓度二硫化碳可引起血总胆固醇升高。     

二硫化碳染毒对大鼠尿酶活性的影响

大量研究表明,CS_2是一种以神经、心血管系统毒性为主的全身性毒物。有关CS_2肾脏毒性的研究报道不多,特别是以尿酶为指标观察CS_2对肾脏损害尚未见报道。为此,本文通过对大鼠进行亚慢性染毒,主要从尿酶活性变化的角度探讨了CS_2对肾脏的毒性作用。材料和方法一、动物分组及染毒:选用体重200±20g健康Wistar火鼠48只,随机分4组,每组12只,雌雄各     

氟砷染毒对大鼠子代脂质过氧化的影响

目的 为揭示氟砷共存时对子代健康影响提供有价值的资料。方法 采取两代一窝繁殖实验的方法,测定Ｗｉｓｔａｒ大鼠暴露于氟砷后其子代血液中脂质过氧化水平和抗氧化能力。要随着暴露剂量的增加,超氧化物歧化酶（ＳＯＤ）和谷胱甘肽过氧化物酶活性随之降低,而脂质过氧化物（ＬＰＯ）含量却逐渐增加,Ｆ２代ＳＯＤ活性在不同的剂量组分别为１４．５６、１３．７４、１１．８９和１１．２１μｍｏｌ．ｍｉｎ＾－１．ｍｇＨｂ＾－１     

二硫化碳染毒雌性大鼠对促性腺激素释放激素刺激反应的研究

二硫化碳 ( CS2 )是工业上广泛使用的一种有机溶剂。近二十年来 ,大量的研究发现 ,CS2 对女性及雌性动物性腺具有损害作用。不少研究认为 ,CS2 对下丘脑 -垂体 -卵巢轴平衡功能的影响是其性腺毒性的重要机制 [1 - 3]。有人认为 ,接触 CS2 女工的血清中 L H水平明显降低可能是由于 CS2 对垂体造成损伤所致[2 ] ;经腹腔给予 CS2 的大鼠垂体促性腺细胞结构 -机能发生改变 [3]。目前国内外对 CS2 染毒对促性腺激素释放激素( Gn RH)刺激反应影响的研究报道甚少。本研究旨在通过对雌性大鼠高、低不同剂量 CS2 染毒进行亚慢性毒性实验 ,测…     

西红花籽油对大鼠脂质代谢的影响

目的：研究西红花籽油对实验性高脂血症大鼠脂质代谢的影响。方法：采用高血脂模型法进行本次研究。结果：10．0mg/kg、3．3ml／kg体重剂量组均能明显降低高脂血症大鼠血清胆固醇(代)和低密度脂蛋白胆固醇(LDL-C)含量，10．0ml／kg体重剂量组能明显降低高脂血症大鼠血清甘油三脂(TG)含量、肝体比和致动脉粥样硬化指数(AI)。结论：西红花籽油具有调节血脂的作用。     

灵芝黑木耳粉对太鼠脂质代谢影响的研究

目的：研究灵芝黑木耳粉对实验性高脂血症大鼠脂质代谢的影响,探索通过饮食来控制血脂的新方法。方法：采用高血脂模型法。结果：3．0g／k、2．0g／kg体重剂量组均能明显降低高脂血症大鼠血清胆固醇(TC)和血清甘油三酯(TG)含量。3．0g／kg体重剂量组能明显降低高脂血症大鼠血清低密度脂蛋白胆固醇(LDL-C)含量。结论：灵芝黑木耳粉具有促进脂质代谢,降低血脂的作用。     

二硫化碳致脂质过氧化作用对心血管的影响

本文观察了二硫化碳(CS_2)腹腔注射染毒35天对大鼠血液、心肌、主动脉中质脂过氧化物(LPO)含量和超氧化物歧化酶(SOD)活性的影响。结果显示:染毒组血清、主动脉中LPO含量比对照组明显增加(P<0.05),心肌中LPO含量也呈明显增加趋势。而各实验组红细胞、心肌和主动脉中SOD活性等无显著性差异(P>0.05)。结果表明,CS_2是一个重要的致脂质过氧化毒物。     

锰缺乏对饲高胆固醇膳食大鼠脂质代谢的影响

目的了解锰缺乏对饲高胆固醇膳食大鼠脂质代谢的影响.方法用雄性刚断乳的Wistar大鼠研究,采用2×2析因设计.结果(1)膳食锰缺乏时,大鼠血清及肝脏甘油三酯含量明显升高(P＜0.01),大鼠出现明显的高甘油三酯血症;(2)膳食锰缺乏与高胆固醇对血脂具有交互作用,高膳食胆固醇加大了锰缺乏对大鼠血脂的影响(交互作用P＜0.01).结论锰缺乏可以造成大鼠脂质代谢的紊乱,锰缺乏可能与动脉粥样硬化的形成有关.     

Hepatic cholesterol metabolism following exposure to carbon disulfide in phenobarbital-treated rats

Male F344 rats were exposed either to 1.87 mg/L (600 ppm) carbon disulfide (CS₂) for 6 hr/day by inhalation for 1, 2, or 3 consecutive days, or to 0.1% phenobarbital (PB) in the drinking water starting 5 days before exposure to CS₂, or to both. Combined treatments (CS₂ + PB) resulted in a decrease in hepatic cholesterol synthesis, increases in hepatic cholesterol concentration and relative liver weight, and histopathologic damage. Maximal inhibition of cholesterol synthesis was observed following 1 day of combined treatments, while the increases in hepatic cholesterol concentration were similar following 1, 2, or 3 days of combined treatments. Exposure to CS₂ only produced a pattern of inhibition of cholesterol synthesis that was similar to, though less extensive than, that seen following combined treatments. All reported alterations caused by combined treatments of CS₂ + PB were reversible; recovery was, in all cases, essentially complete by day 11 after a single exposure to 1.87 mg/L CS₂. With the exception of cholesterol concentration where time to recovery was decreased by continuation of PB, the time required for recovery from the effects of combined treatments of CS₂ + PB was not affected by whether or not PB was continued after CS₂ exposure. The reported observations support the theory that metabolism of CS₂ is involved in the expression of CS₂-mediated alterations of hepatic cholesterol metabolism.     

Occupational exposure to low concentrations of carbon disulfide as a risk factor for hypercholesterolaemia

OBJECTIVE: The objective of this study was to investigate the effect of occupational exposure to carbon disulfide (CS2) concentrations below threshold limit value (TLV)-time-weighted average (TWA) (31 mg/m3) on total cholesterol, blood pressure and the prevalence of coronary heart disease (CHD). METHODS: A cross-sectional study involving 141 viscose rayon workers (64 men), and 141 age- and gender-matched controls without occupational contact with noxious chemicals, was carried out. The probability for CHD was determined by means of the WHO questionnaire and was 12-lead electrocardiography-coded using Minnesota criteria. Blood pressure was measured by the standardized method of the WHO and blood was examined for total cholesterol. A cumulative exposure index (CS2 index) was calculated for each worker by multiplying the number of years held in a particular job, by the CS2 concentrations in that job-environment. According to the CS2 index, the exposed workers were distributed into two groups: group 1 (CS2 index < 100) and group 2 (CS2 index > or = 100). RESULTS: Depending on the job and specific work place the CS2 concentrations were between 1 and 30 mg/m3. Cholesterol levels were significantly higher in the exposed group (4.9 +/- 0.7) compared with the controls (4.6 +/- 0.7). Adjustment for age, smoking, body-mass index (BMI) and gender showed the significant effect of the CS2 index on the total cholesterol (P < 0.001). The prevalence of hypercholesterolaemia was significantly higher in the exposed group (42.6%), compared with the controls (26.2%); odds ratio (OR) (adjusted for potential confounders) was 2.56, 95% CI 1.47-4.46. Logistic regression showed a significantly increased risk for elevated cholesterol in group 2 (OR 5.52; 95% CI 2.81-10.83). No significant effect of CS2 index on blood pressure and CHD prevalence was found. CONCLUSIONS: The results of our study show that occupational exposure to CS2 concentrations below 31 mg/m3 and a CS2 index > 100 may increase total cholesterol. Our results imply that even the CS2 concentrations below TLV-TWA may produce morbid changes, and suggest the mechanism of the effect of CS2, leading to lipid metabolism disturbances and acceleration of atherosclerosis.     

Occupational exposure to low concentrations of carbon disulfide as a risk factor for hypercholesterolaemia

Objective: The objective of this study was to investigate the effect of occupational exposure to carbon disulfide (CS₂) concentrations below threshold limit value (TLV)-time-weighted average (TWA) (31 mg/m³) on total cholesterol, blood pressure and the prevalence of coronary heart disease (CHD). Methods: A cross-sectional study involving 141 viscose rayon workers (64 men), and 141 age- and gender-matched controls without occupational contact with noxious chemicals, was carried out. The probability for CHD was determined by means of the WHO questionnaire and was 12-lead electrocardiography-coded using Minnesota criteria. Blood pressure was measured by the standardized method of the WHO and blood was examined for total cholesterol. A cumulative exposure index (CS₂ index) was calculated for each worker by multiplying the number of years held in a particular job, by the CS₂ concentrations in that job-environment. According to the CS₂ index, the exposed workers were distributed into two groups: group 1 (CS₂ index <100) and group 2 (CS₂ index ≥100). Results: Depending on the job and specific work place the CS₂ concentrations were between 1 and 30 mg/m³. Cholesterol levels were significantly higher in the exposed group (4.9 ± 0.7) compared with the controls (4.6 ± 0.7). Adjustment for age, smoking, body-mass index (BMI) and gender showed the significant effect of the CS₂ index on the total cholesterol (P < 0.001). The prevalence of hypercholesterolaemia was significantly higher in the exposed group (42.6%), compared with the controls (26.2%); odds ratio (OR) (adjusted for potential confounders) was 2.56, 95% CI 1.47–4.46. Logistic regression showed a significantly increased risk for elevated cholesterol in group 2 (OR 5.52; 95% CI 2.81–10.83). No significant effect of CS₂ index on blood pressure and CHD prevalence was found. Conclusions: The results of our study show that occupational exposure to CS₂ concentrations below 31 mg/m³ and a CS₂ index >100 may increase total cholesterol. Our results imply that even the CS₂ concentrations below TLV-TWA may produce morbid changes, and suggest the mechanism of the effect of CS₂, leading to lipid metabolism disturbances and acceleration of atherosclerosis. Received: 1 February 2000 / Accepted: 24 June 2000     

Experimental human exposure to carbon disulfide

Summary Six human volunteers were exposed to 10 and 20 ppm carbon disulfide at rest and to 3 and 10 ppm carbon disulfide under a 50 W level of physical exercise during four consecutive periods of 50 min. At the start of the experiments, at the end of the exposure periods and during the post-exposure period, urine was sampled and the concentration of 2-thiothiazolidine-4-carboxylic acid (TTCA) was determined. It was established that only a small percentage, ranging from 0.7 to 2.2% of the absorbed carbon sulfide was transformed into TTCA. The excretion rate of TTCA (mol TTCA h^–1) was found to be the best parameter in evaluating the respiratory uptake of carbon disulfide over a range of 37.9 to 163.3 mg CS₂ compared to the urinary concentration of TTCA (mole TTCA ml^–1) or the creatinine corrected concentration of TTCA (mmol TTCA mol^–1 creatinine). The total amount of TTCA (mol TTCA) excreted proved to be independent of the urinary flow (ml h^–1), the estimates of the individual fatty tissue content and the urinary pH. No correlation was found between the respiratory uptake of carbon disulfide (mg CS₂) and the excretion rate of TTCA within each exposure condition of 3, 10 or 20 ppm carbon disulfide, respectively.