Structural and functional changes in organelles of liver cells in rats exposed to magnetic fields.

Exposure of rats to magnetic fields of 10(-3) and 10(-2) T for 1 hr daily generated structural changes in hepatocytes mitochondria, endoplasmic reticulum, and ribosomes. Simultaneously there was an increase in the activities of the mitochrondrial respiratory enzymes: NADH dehydrogenase, succinic dehydrogenase, and cytochrome oxidase. The extent of the changes in liver cell properties following exposure depend on the duration of exposure to and the strength of the applied magnetic fields. Ultrastructural studies did not reveal any changes in external membranes of hepatocytes or in the membranes of cell nuclei. An increase in the amount of glycogen in hepatocytes of rats exposed to both 10(-3) and 10(-2) T was noted. The high level of cortisol in serum of exposed rats suggests that magnetic field may be a stress generating factor.     

Acetaldehyde and alcohol levels in pregnant rats and their fetuses

Alcohol and acetaldehyde blood levels were measured in chronic alcoholic pregnant rats and their fetuses at 15, 19 and 21 days of gestation. Similar ethanol concentrations were found in fetal and maternal blood in all gestation periods studied, however levels in amniotic fluid were higher than in mother's blood, especially in the early stages of gestation. Acetaldehyde concentrations were always lower in fetal than in maternal blood although increasing throughout gestation. The levels in fetal blood and amniotic fluid compared to maternal blood, were ca. 40, 50 and 70% at 15, 19 and 21 days of gestation, respectively; those for the placenta and fetal tissues were lower, i.e., 25, 40 and 50%. Similar alcohol and acetaldehyde ratios (fetus/mother's concentration) were obtained when pregnant non-alcoholic rats were administered cyanamide and ethanol (2 g/kg) at 11, 15, 19 and 21 days of gestation. These results demonstrate that ethanol freely crosses the placental barrier, but there is a concentration gradient of acetaldehyde between mother and fetus which varies with gestation age.     

铅对怀孕大鼠及其胎鼠肝脏脂质过氧化的影响

目的 探讨铅对母鼠及胎鼠肝脏损伤的机制。方法 雌性大鼠于怀孕前经饮水染铅1个月,受孕后仍持续染铅,于孕第20天处死,取母鼠及胎鼠的血和肝脏,测定血铅、肝组织脂质过氧化（LPO）水平及相关抗氧化指标。结果 （1）随着饮水中铅含量的增加,母鼠及胎鼠血铅含量均增加,胎鼠血铅负荷达到母鼠水平;（2）肝组织LPO水平在母鼠0.2%组及胎鼠0.05%、0.2%组显著高于对照组;（3）还原型谷胱甘肽（GSH）含量在母鼠与胎鼠0.05%、0.2%组显著增高,谷胱甘肽过氧化物酶（GSH-Px)含量则显著降低。结论 铅可使孕鼠及其胎鼠肝脏脂质过氧化作用增强,并可能通过脂质过氧化作用而影响胚胎发育,胎鼠对铅的毒性更敏感。     

Influence of ethanol on lead distribution and biochemical changes in rats exposed to lead

In the present study, an attempt has been made to investigate the effect of ethanol consumption on the distribution of lead in different regions of brain and body organs of male albino rats. Lead when administered intragastrically, for a period of eight weeks resulted in almost uniform accumulation of this metal in all the regions of brain, which increased by almost two fold when ethanol was given along with lead. Lead was also seen to compartmentalise in almost all the tissues of the body to varying extents, with the highest accumulation in the kidney. A progressive and appreciable accumulation of lead was seen in blood with a concomitant increase in ZPP levels in animals during the course of treatment, which increased further when ethanol was administered along with lead. The activity of δ-ALAD and AChE in blood was significantly decreased in lead as well as ethanol treated animals. However, in animals coexposed to lead and ethanol, the inhibition of δ-ALAD was not significantly different, when compared to only lead-treated animals. The results suggested that animals exposed to ethanol and lead simultaneously accumulate higher levels of lead in blood and brain of animals making them more vulnerable to the haematological and neurological toxic effects of lead.     

Cadmium content of lung,liver and kidney in rats exposed to cadmium oxide fumes

Summary Young male rats were submitted to five consecutive exposures to atmospheres containing cadmium oxide particles (280 min × mg/m³) and sacrificed at different times of a three months post-exposure period. Time-course evolution of lung, liver and kidney weight as well as cadmium content of these organs were studied by polynomial regression analysis.Growth of lungs was profoundly disturbed in rats exposed to the aerosol and some degree of permanent damage of pulmonary lobes could be evidenced by macroscopic examination. Liver growth was affected to a less extent and no effect on the growth of kidneys was observed.Results showed that 12% of inhaled cadmium are deposited in lungs. Clearance of pulmonary cadmium was slow, exponential and monophasic (half-life 56 days). A slight, but statistically significant, accumulation of the toxic element in liver and kidney was seen.The results suggest that 60% of the lung-deposited cadmium are absorbed.     

Concurrent exposure to lead,manganese, and cadmium and their distribution to various brain regions,liver, kidney,and testis of growing rats

Growing rats were exposed to 5 mg/L Pb,ad libitum in drinking water, and administered low or high doses of Mn and Cd intraperitoneal (i.p.) for 30 days. Some groups of animals were also administered combinations of Pb + Mn and Pb + Cd in an identical manner. Analysis of Pb, Mn, and Cd in tissue samples showed the expected dose-dependent accumulation when the metal was administered singly. However, combined treatment produced different types of metal shift in different tissues. Enhanced accumulation of all three metals in the brain, Mn in liver, Pb in kidney and Cd in testis and kidney after combined exposure may make target organs vulnerable to the toxic effects of metals, even when encountered at low concentrations. Further, the decreased levels of blood Pb after combined treatment with Cd or Mn suggests that the significance of blood Pb level as a diagnostic aid for Pb toxicity in coexposed conditions may not be of much value. Changes in the metallic distribution within the tissues after coexposure may be the result of a competition between the administered metals for common binding sites.     

Weight gain and maturity in fetuses exposed to low levels of lead

The relationship between prenatal low-level lead exposure and fetal growth was evaluated in a sample of 4354 pregnancies in which the mean umbilical cord blood lead level was 7.0 micrograms/dl (SD = 3.3; 10th percentile, 3.4 micrograms/dl, 90th percentile, 10.9 micrograms/dl). Higher cord blood lead levels were significantly associated with gestations of slightly longer duration. Comparing infants with cord blood lead levels greater than or equal to 15 micrograms/dl to those with levels less than 5 micrograms/dl, adjusted risk ratios of 1.5 to 2.5 were observed for low birth weight (less than 2500 g) and for fetal growth indices that express birth weight as a function of length of gestation (e.g., small-for-gestational age, intrauterine growth retardation). The 95% confidence intervals of these risk ratios included 1, however, precluding rejection of the null hypothesis of no association. We conclude that the risk of adverse fetal growth is not increased at cord blood lead levels less than 15 micrograms/dl but that modest increases in risk may be associated with levels greater than or equal to 15 micrograms/dl.     

Effect of the herbicide glyphosate on enzymatic activity in pregnant rats and their fetuses

To prevent health risk from environmental chemicals, particularly for progeny, we have studied the effects of the herbicide glyphosate on several enzymes of pregnant rats. Glyphosate is an organophosphorated nonselective agrochemical widely used in many countries including Argentina and acts after the sprout in a systemic way. We have studied three cytosolic enzymes: isocitrate dehydrogenase-NADP dependent, glucose-6-phosphate dehydrogenase, and malic dehydrogenase in liver, heart, and brain of pregnant Wistar rats. The treatment was administered during the 21 days of pregnancy, with 1 week as an acclimation period. The results suggest that maternal exposure to agrochemicals during pregnancy induces a variety of functional abnormalities in the specific activity of the enzymes in the studied organs of the pregnant rats and their fetuses.     

Organ and subcellular distribution of cadmium in rats exposed to cadmium, mercury, and selenium

Four groups of rats were given: cadmium chloride (Cd), cadmium chloride and mercuric chloride (Cd + Hg), cadmium chloride and sodium selenite (Cd + Se), or cadmium chloride, mercuric chloride, and sodium selenite (Cd + Hg + Se). All animals received subcutaneous doses of 115mCdCl2 (0.3 mg Cd/kg) every other day for 2 weeks. Mercuric chloride was administered intravenously at doses of 0.5 mg Hg/kg every other day, and Na2 75SeO3 intragastrically at doses of 0.1 mg Se/kg every day for a fortnight. The whole-body and organ retention of cadmium changed slightly with the type of exposure. A significant interaction effect of the examined elements was noted in the nuclear and soluble fractions of the liver and kidneys. Mercury decreased the cadmium concentration in both the nuclear and soluble fractions of the kidneys and diminished the effect of selenium on the cadmium level in the soluble fraction of the kidneys. In the liver the presence of mercury contrary to selenium, lowered the cadmium level in the nuclear fraction. The pattern of cadmium binding to proteins of the soluble fraction of the kidneys and liver remained the same in all groups of animals.     

铅、镉、砷污染地区人群免疫功能检测分析

目的探讨铅锌矿矿区铅镉砷混合接触对不同暴露人群机体免疫状况的影响。方法选择铅锌矿矿区矿工、矿区居民和无污染地区居民3组人群共96人作为研究对象,对3组人群所处环境中的铅、镉、砷含量,人体血液和尿液的铅、镉、砷含量以及人体免疫学指标进行分析。结果矿工组血中铅、镉、砷含量几何均数分别为216.57,5.04,58.65μg/L,矿区居民组血中铅、镉、砷含量几何均数分别为143.62,2.42,33.24μg/L,均高于对照人群,几何均数分别为81.54,1.18,11.50μg/L(P<0.01)。3组人群尿液中的各种毒物差异有统计学意义(P<0.01)。矿工和矿区居民的免疫功能相对于对照组均有不同程度的下降(P<0.01)。结论接触铅、镉和砷的矿区矿工和居民免疫功能受到了不同程度的损害。     

宫内铅暴露的行为畸胎学毒性及脑海马神经化学的改变

以大鼠为动物模型 ,应用行为畸胎学方法观察了出生前接触铅对胎鼠出生后生长发育、行为能力和学习记忆功能等的毒效应 ,并测定了仔鼠脑海马组织中胆碱乙酰转移酶 (ChAT)活性和兴奋性氨基酸神经递质谷氨酸 (Glu)和门冬氨酸 (Asp)含量的变化 ,拟探讨上述损害可能涉及的生化基础。实验动物随机分为 :对照组 ,饮用去离子水 ;低铅组 ,饮用 0 5g L醋酸铅水 ;高铅组 ,饮用 2g L醋酸铅水 ;染铅从交配前 10天开始直到断乳。结果显示 ,与对照组相比 ,低铅组仔鼠睁眼时间延迟 ;高铅组仔鼠耳廓分离、出毛、门齿萌出、张耳及平面翻正等指标发育延迟 ;跳台试验中 ,2 1日及 35日龄铅暴露组动物出现错误反应的次数明显增多 ;中毒组仔鼠 2 1日及 35日龄时脑海马组织ChAT活性、Glu和Asp含量均明显低于对照组的。该结果提示 ,出生前低铅暴露导致的大鼠胆碱能系统及谷氨酸能系统状态低下与铅的神经行为学毒性相关联     

Fertility of male workers exposed to cadmium, lead, or manganese.

The effect of exposure to cadmium, lead, or manganese on male reproductive function was examined in 1988-1989 in Belgian blue-collar workers. The workers were exposed to cadmium in two smelters (n = 83; geometric mean urinary cadmium level = 6.94 micrograms/g of creatinine; mean duration of exposure = 24 years), to lead in a battery factory (n = 74; mean blood lead level = 46.3 micrograms/dl; mean duration of exposure = 10.7 years), or to manganese (manganese dioxide) in a dry alkaline battery plant (n = 70; median atmospheric concentration of total manganese dust = 0.71 mg/m3; mean duration of exposure = 6.2 years). Fertility in these workers and in an unexposed population (n = 138) was assessed by examining the birth experiences of their wives through a logistic regression model. The probability of a live birth was not different between the unexposed workers and the cadmium- or manganese-exposed workers before or after the onset of exposure. While the fertility of the lead-exposed workers was somewhat greater than that of the unexposed before the onset of exposure, a significant decrease in fertility was observed during the period of exposure to the metal (odds ratio = 0.65, 95% confidence interval 0.43-0.98).     

Alterations in the activity of some digestive enzymes ofChanna punctatus,exposed to lead nitrate

Summary The effect of exposure ofChanna punctatus to a sub-lethal concentration of lead nitrate on the activities of alkaline phosphatase, acid phosphatase amylase, maltase, lactase, trypsin and pepsin has been investigated. A decrease in the activity of alkaline phosphatase has been recorded after 15 days of exposure but there was no significant change after 30 days. Acid phosphatase showed an elevation in activity of both stages. All the three carbohydrases shows elevation after 15 days, followed by an inhibition after 30 days of treatment. The activity of pepsin and trypsin remained above the normal level throughout the tenure of the experiment reveal that the pattern of alteration in enzyme activities is different in liver and digestive system.     

Urinary kallikrein activity in workers exposed to cadmium, lead, or mercury vapour

A significant reduction of kallikrein activity in urine (assayed by its amidolytic activity) was found in 64 normotensive workers who had been exposed to cadmium for 11 years on average and whose cadmium concentrations in urine ranged from 2.2 to 33.1 micrograms/g creatinine. The mean (geometric) urinary kallikrein activity (in U/g creatinine) amounted to 0.52 (range 0.11-1.90) in the control group (n = 193) against 0.39 (range 0.10-1.03) in the cadmium group, and the prevalence of abnormally low activity levels (less than or equal to 0.20 U/g creatinine) amounted to 17.2% in the cadmium group against 5.2% in the control group. A reduction of aldosterone release (aldosterone in urine) associated with an increased natriuresis was also observed. This might constitute a compensatory mechanism maintaining blood pressure in the normal range. These biological effects of cadmium were not reversible after removal from exposure. This study indicates that cadmium can induce an irreversible toxic effect in the distal nephron. It also suggests that an excessive cadmium body burden alone may not be sufficient to induce hypertension, but in individuals whose blood pressure regulation may be impaired by other factors cadmium could stimulate the development of hypertension. This study also supports the recommendation to prevent hypertensive subjects from being exposed to cadmium. There was no indication that moderate exposure to mercury vapour (n = 53; mercury in urine, range 11-224 micrograms/g creatinine; average duration of exposure: six years) or to inorganic lead (n = 23; lead in blood, range 40-67 micrograms/100 ml; average duration of exposure: eight years) was associated with a reduction of kallikrein production by the kidney.     

Biotransformational and neurophysiological changes in rabbits exposed to lead

Lead was administered to adult male rabbits in drinking water at a 0.1% concentration for four and five week periods. The lead contents were determined in the central and peripheral nervous tissues and in the liver, kidney, and intestinal mucosa. The conduction velocity of sciatic nerve and the activities of drug metabolizing enzymes in other tissues were determined. The lead concentration in the blood was at a steady state at four to five weeks of exposure. Lead accumulated in all tissues except the brain. The brain lead concentration was 40 to 50% of that in the blood, indicating the existence of a blood-brain barrier. However, the lead concentration in the sciatic nerve increased significantly from four to five weeks of exposure and exceeded that in the blood. This indicates the lack of a blood-nervous tissue barrier in the sciatic nerve allowing a continuous accumulation of lead. This accumulation affected the function of the sciatic nerve; motor nerve conduction velocity decreased from the control level (58.3±7.4 m/sec) to 43.8±6.3 m/sec after the four-week exposure and to 35.0 ± 1.3 m/sec at 5 weeks of exposure. After five weeks of exposure, no changes in the hepatic, intestinal, or renal drug metabolizing enzyme activites were found. These results suggest that motor nerve conduction velocity is affected by lead exposure prior to any influence on biotransformation enzymes.     

Urinary kallikrein activity in workers exposed to cadmium, lead, or mercury vapour.

A significant reduction of kallikrein activity in urine (assayed by its amidolytic activity) was found in 64 normotensive workers who had been exposed to cadmium for 11 years on average and whose cadmium concentrations in urine ranged from 2.2 to 33.1 micrograms/g creatinine. The mean (geometric) urinary kallikrein activity (in U/g creatinine) amounted to 0.52 (range 0.11-1.90) in the control group (n = 193) against 0.39 (range 0.10-1.03) in the cadmium group, and the prevalence of abnormally low activity levels (less than or equal to 0.20 U/g creatinine) amounted to 17.2% in the cadmium group against 5.2% in the control group. A reduction of aldosterone release (aldosterone in urine) associated with an increased natriuresis was also observed. This might constitute a compensatory mechanism maintaining blood pressure in the normal range. These biological effects of cadmium were not reversible after removal from exposure. This study indicates that cadmium can induce an irreversible toxic effect in the distal nephron. It also suggests that an excessive cadmium body burden alone may not be sufficient to induce hypertension, but in individuals whose blood pressure regulation may be impaired by other factors cadmium could stimulate the development of hypertension. This study also supports the recommendation to prevent hypertensive subjects from being exposed to cadmium. There was no indication that moderate exposure to mercury vapour (n = 53; mercury in urine, range 11-224 micrograms/g creatinine; average duration of exposure: six years) or to inorganic lead (n = 23; lead in blood, range 40-67 micrograms/100 ml; average duration of exposure: eight years) was associated with a reduction of kallikrein production by the kidney.     

Structural and functional changes in gill mitochondrial membranes from the Mediterranean mussel Mytilus galloprovincialis exposed to tri-n-butyltin

The use of tributyltin (TBT) as a biocide in antifouling paints leads to a ruinous input of this contaminant in the aquatic environment. Human exposure to TBT mainly occurs through ingestion of contaminated seafood such as filter-feeding mollusks. Tributyltin is known to act as a membrane-active toxicant on several targets, but especially on the mitochondria, and by several mechanisms. The effects of tributyltin on fatty acid composition, on Mg-adenosine triphosphatase (ATPase) activities, and on the membrane physical state were investigated in gill mitochondrial membranes from cultivated mussels Mytilus galloprovincialis exposed to 0.5 μg/L and 1.0 μg/L TBT and unexposed for 120 h. The higher TBT exposure dose induced a decrease in the total and n-3 polyunsaturated fatty acids (PUFAs), especially 22:6 n-3, and an activation of the oligomycin-sensitive Mg-ATPase. Both TBT concentrations decreased mitochondrial membrane polarity detected by Laurdan steady-state fluorescence spectroscopy. These findings may help cast light on the multiple modes of action of this toxicant.     

Mitogen stimulation of lymphocytes in CBA mice exposed to lead and cadmium.

CBA mice were exposed to lead acetate or cadmium chloride in drinking water for 10 weeks. Selected groups of these animals were also injected with Bacillus Calmette-Guerin (BCG) during exposure to the metals. The ability of mitogens concanavalin A (Con A) and lipopolysaccharide (LPS) as well as purified protein derivative (PPD) to induce proliferation of splenic lymphocytes was assessed. In general, lead tended to inhibit lymphocyte proliferation by LPS and PPD while cadmium potentiated blastogenesis by these mitogens. The two larger doses of cadmium, 30 and 300 ppm, resulted in intense proliferation which was significant (P < 0.05) for the non-BCG, 300-ppm cadmium group. However, 3 ppm cadmium reduced the lymphocyte response to LPS and PPD which was significant (P < 0.05) for the non-BCG-injected mice. Lead and cadmium did not significantly affect the response of lymphocyte proliferation by Con A. Group variation and interpretation of data are discussed.