Effectiveness of ZnCl2 in protecting against nephrotoxicity induced by HgCl2 in newborn rats

This work investigated the preventive effects of ZnCl₂ on renal and hepatic alterations induced by HgCl₂ in young rats. Wistar rats of 3 days old were treated (s.c.) on consecutive days with saline or ZnCl₂ 27 mg/kg/day from the 3rd to the 7th and with saline or HgCl₂ 5.0 mg/kg/day from the 8th to the 12th day of life. Pups were sacrificed 24 h after the last dose and samples were collected. The creatinine and urea dosages, used as renal parameters, presented increases of 35% and 500%, respectively. The alanine aminotransferase and lactic dehydrogenase activities, used as hepatic parameters, presented a decrease (40%) and no alteration, respectively, by mercury exposure. The glycemia was diminished and the hepatic glycogen was not modified by mercury. All the mercury effects were prevented by zinc. These results suggest that mercury intoxication of young rats alters the renal function but does not modify the hepatic parameters, and previous exposure to zinc is able to avoid the renal damage.     

Metabolic alterations in liver and kidney following chronic methyl mercury treatment and withdrawal

Daily intraperitoneal injection of methyl mercury (0.4 and 4 mg/kg) for 45 days to rats decreased liver size without producing any significant change in adrenal, cardiac, renal, testicular, and body weight. Chronic exposure to either dose of this organomercurial augmented the activities of renal and hepatic pyruvate carboxylase, phosphoenolpyruvate carboxykinase, fructose 1,6-diphosphatase and glucose 6-phosphatase, elevated the concentration of blood glucose and urea, as well as reduced liver glycogen content. As expected, the degree of alterations in various parameters studied was greater in animals which were injected with the higher dose (4 mg/kg) of methyl mercury. Furthermore, withdrawal of treatment for 28 days in rats that had previously been given the 4 mg/kg daily dose of methyl mercury for 45 days, generally failed to reverse the observed metabolic changes in hepatic and renal carbohydrate metabolism. Our results suggest that the gluconeogenic potential of both liver and kidney is markedly enhanced in animals chronically treated with methyl mercury and that the metabolic alterations persist even after a 28 day period of abstinence from heavy metal treatment.     

Ameliorative effect of melatonin against gamma-irradiation-induced oxidative stress and tissue injury

While radiation hazards, due to free radical generation, present an enormous challenge for biological and medical safety, melatonin is a potent scavenger of a variety of free radicals. The aim of this study was to investigate the radioprotective effect of melatonin against oxidative stress and tissue injury induced by gamma radiation. Rats were subjected to two doses of 2 and 4Gy from cesium-137 source. Four days prior to irradiation, animals received melatonin daily (10mg/kg body weight i.p.). In the irradiated animals, the oxidative stress markers malondialdehyde (MDA) and protein carbonyl were significantly increased in the liver, while a marked decrease in hepatic contents of DNA, RNA, and glutathione (GSH) as well as activity of glutathione-S-transferase (GST) was demonstrated. In addition, catalase (CAT) activity was increased in the liver 5 days after irradiation. The levels of total lipids, cholesterol, triglyceride (TG), low-density lipoprotein (LDL), urea, and creatinine, as well as activities of aspartate aminotransferase (AST), alkaline phosphatase (ALP), and gamma-glutamyltransferase (GGT), were significantly increased in sera of the irradiated rats. This is coupled with decreased serum levels of high-density lipoprotein (HDL), total protein and albumin, and total globulins by irradiation. The administration of melatonin alone daily for 4 days caused significant decreases in MDA and protein carbonyl content and produced significant elevations of GSH content and GST activity in the liver. Moreover, significant decreases in total lipids, cholesterol, and TG without change in LDL or HDL levels in serum were demonstrated. Treatment with melatonin for 4 days before acute irradiation significantly abolished radiation-induced elevations in MDA and protein carbonyl levels in the liver and significantly maintained hepatic GSH content, GST, and CAT activities close to the control values. Preirradiation treatment with melatonin showed significantly higher hepatic DNA and RNA contents than irradiated rats. The levels of total lipids, cholesterol, TG, HDL, LDL, total proteins, albumin, total globulins, creatinine, and urea, as well as the activities of AST, ALT, and GGT in serum were significantly ameliorated when melatonin was injected before irradiation. In conclusion, the increase in oxidative stress markers and the concomitant change in antioxidant levels indicate the role of oxidative stress in radiation-induced tissue damage. Moreover, melatonin shows a radioprotective impact against ionizing-radiation-induced oxidative stress and organ injury.     

Chronic toxicity of fumonisins from Fusarium moniliforme culture material (M-1325) to mink

Adult female mink (Mustela vison) were fed a diet that contained Fusarium moniliforme culture material that provided dietary concentrations of 89 ppm fumonisin B₁, 21 ppm fumonisin B₂, and 8 ppm fumonisin B₃ for 87 days. During the trial, there was mild lethargy in the mink fed fumonisins, but no other clinical signs or differences in feed consumption (measured during the first two weeks), body weights, or survivability were observed between the fumonisin-treated and control mink. Several hematologic parameters (mean corpuscular hemoglobin concentration, plasma total solids, and lymphocyte concentration) and serum chemical concentrations (globulin, phosphorus, potassium, blood urea nitrogen, creatinine, bilirubin, and cholesterol) and activities (alkaline phosphatase, alanine aminotransferase, amylase, and aspartate aminotransferase) were greater in the mink fed fumonisins than in the controls. Serum albumin/globulin and sodium/potassium ratios and chloride concentrations were lower in the fumonisin-fed mink than in the controls. The concentrations of free sphinganine and the ratio of free sphinganine to free sphingosine in the liver and kidneys of the fumonisin-treated mink were greater than in the control mink. No histopathologic alterations were associated with fumonisin treatment. These results indicate that long-term dietary exposure to F. moniliforme culture material containing 118 ppm total fumonisins is not lethal to adult mink, but can produce adverse physiological effects in the animals.     

Liver and kidney function and histology in rats exposed to cadmium and ethanol

AIMS: The present study was performed to assess the function and histology of the liver and kidney in rats exposed to 50 mg Cd/l (as cadmium chloride) and/or 10% (w/v) ethanol (EtOH) for 12 weeks. METHODS: The activities of alanine aminotransferase (ALAT) and asparate aminotransferase (AspAT) in serum were measured as indicators of the liver function. As parameters of the kidney function, creatinine, total protein and urea concentrations in serum and urine, as well as urinary alkaline phosphatase (ALP) activity were determined, and creatinine clearance was calculated. Both organs were subjected to histopathological analysis. RESULTS: Daily Cd intake ranged from 3.17 to 4.28 mg/kg body weight and from 2.41 to 3.17 mg/kg body weight in the Cd and Cd + EtOH groups, respectively. The daily intake of 10% EtOH ranged from 47.5 to 86.9 g/kg body weight in the EtOH and from 47.3 to 63.4 g/kg body weight in the Cd + EtOH-exposed rats. Cd and EtOH, independently of separate or combined application, changed liver and kidney function and histology. Rats treated with Cd alone and those co-exposed to both substances showed qualitatively similar, but different magnitudes of changes, in liver and kidney histology. Blurred trabecular structure, vacuolar degeneration and increased density of nuclear chromatin with very compact nuclear structure were found in hepatocytes of zones 2 and 3. Moreover, mononuclear cell infiltrations and necrosis of single cells were evident in zone 1. In the kidney tubules, degeneration and hypertrophy of epithelial cells and dilation in the glomeruli were also observed. Some functional (increased serum AspAT and urinary ALP, decreased urinary urea) and structural changes in the liver and kidney were more evident in the case of combined exposure, while others were more evident after single exposure. However, a decrease in creatinine clearance, noted only in the animals treated with Cd and EtOH, shows that functional changes indicating renal insufficiency are more serious in the co-exposed group. CONCLUSIONS: Due to lower Cd and EtOH intake (resulting from a stronger aversion to drinking water containing both substances) in the co-exposed rats, as compared to the Cd- and EtOH-treated groups, it is difficult to draw a definite conclusion from this study. The findings, however, seem to indicate that EtOH increases Cd nephrotoxicity in rats, and thus may suggest a higher risk of kidney damage in alcoholics exposed to Cd. Unfortunately, this study does not provide clear evidence if, and to what extent, EtOH influences Cd hepatotoxicity.     

沙棘油对汞致急性肝、肾损伤的保护作用

[目的]探讨急性染汞致大鼠肝、肾毒性的作用机制,观察沙棘油（SBO）的保护作用。[方法]24只Wistar大鼠随机均分为：阴性对照组（皮下注射0．9％生理盐水）;染汞组（皮下注射2．5mg／kgHgCl：）;SBO＋HgCl2组[灌胃SBO（体积分数为95％）5mL／kg,2h后皮下注射2．5mg／kgHgCl2］。染汞后12h将大鼠移入代谢笼,收集12h尿样。染汞48h后处死,采取血样和肝肾组织。测定肝脏、肾皮质和尿汞含量;尿N-乙酰-β—D-氨基葡萄苷酶（NAG）、碱性磷酸酶（ALP）、乳酸脱氢酶（LDH）活性和尿蛋白、血清尿素氮（BUN）含量;肝、肾中谷胱甘肽（GSH）、丙二醛（MDA）、蛋白含量和超氧化物岐化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）活性。[结果]与对照组相比,HgCl2组、SBO＋HgCl2组的肝、肾皮质及尿汞含量均明显增加（P〈0．01）;与HgCl2组相比,SBO＋HgC｜2组尿汞含量增加（P〈0．05）。HgCl2组尿NAG、ALP、LDH活性和尿蛋白、BUN含量均明显高于对照组（P〈0．01）;SBO＋HgCl2组NAG、ALP活性和BUN含量均低于HgCl2组（分别为P〈0．05,P〈0．01和P〈0．01）。与对照组相比,HgCl2组肝、肾GSH含量、GSH—Px活性、SOD活性均下降（P〈0．01）,MDA含量增加（P〈0．05或P〈0．01）;SBO＋HgCl2组与HgCl2组相比,其肝GSH-Px活性明显增加（P〈0．01）。[结论]大鼠经一次染汞后可致急性肝、肾损伤。沙棘油具有促进汞从肾脏排出的作用,对汞致肝脏氧化损伤有一定保护作用。     

亚硒酸钠对镉和汞肝肾氧化损伤影响的实验研究

目的:观察一次染镉和汞对大鼠肝、肾组织氧化损伤作用,探讨亚硒酸钠预处理对镉和汞氧化损伤的影响。方法:Wister大鼠48只,随机分成6组,每组8只,第1组为染镉实验对照组,第2组为单纯染镉组,第3组为亚硒酸钠预处理组,第4组为染汞实验对照组,第5组为单纯染汞组,第6组为亚硒酸钠预处理干预组。第1、4组大鼠先腹腔注射生理盐水,2 h后皮下注射生理盐水。第2组大鼠先腹腔注射生理盐水,2 h后皮下注射35μmol/kg氯化镉溶液。第3组大鼠先腹腔注射10μmol/kg亚硒酸钠溶液,2 h后皮下注射35μmol/kg氯化镉溶液。第5组大鼠先腹腔注射生理盐水,2 h后皮下注射2.5 mg/kg HgCl2溶液,第6组大鼠先腹腔注射20μmol/kg亚硒酸钠溶液,2 h后皮下注射2.5 mg/kg HgCl2溶液。染毒24 h后测定肝、肾皮质镉或汞、谷胱甘肽、丙二醛含量和谷胱甘肽过氧化物酶活性。结果:与对照组比较,单纯染镉组大鼠肝GSH、MDA含量显著升高,GSH—Px活性显著下降。Na2SeO3预处理组肝、肾皮质GSH和镉含量显著降低,肝脏GSH—Px活性及肾皮质MDA含量显著升高。单纯染汞组大鼠肝、肾皮质及尿汞含量均显著高于对照组。单纯染汞组肝MDA含量显著高于对照组,GSH含量和GSH—Px活性显著低于对照组。Na2SeO3预处理组的肝脏GSH含量和GSH—Px活性均较单纯染汞组升高,有显著性差异。单纯染汞组肾皮质MDA含量显著高于对照组,GSH含量和GSH—Px活性显著降低。Na2SeO3预处理组中肾皮质MDA含量低于单纯染汞组,GSH—Px含量高于单纯染汞组。结论:给大鼠一次染镉和汞,可以对肝和肾脏产生明显的氧化损伤作用。亚硒酸钠对急性染镉和汞所致肝肾损伤具有一定的拮抗作用,其机制可能与增加内源性GSH、使GSH—Px活性增强以及清除自由基能力提高有关。     

氯化汞对小鼠肾脏的急性毒性机制探讨

目的 进一步探讨氯化汞对肾脏的毒性及作用机制。方法 分别测定氯化汞染毒小鼠的血清肌酐（Cr)和尿素氮（BUN）、肾脏脂质过氧化物（LPO）值及肾脏汞、钙、铁、锌、铜等金属浓度和肾脏组织形态的变化。结果 染毒组小鼠上述指标及肾脏组织形态与对照组相比,差异均有显著性。结论 氯化汞具有明显的肾脏毒性,诱发脂质过氧化增强及引起钙、铁、锌、铜等微量元素代谢障碍可能是氯化汞引起肾脏损伤的重要因素。     

Differential oxidative stress responses to methanol in intraperitoneally exposed rats: ameliorative effects of Opuntia vulgaris fruit extract

Methanol is primarily metabolized by oxidation to formaldehyde and then to formate. These processes are accompanied by formation of superoxide anion and hydrogen peroxide. This article reports data on the effect of methanol-induced oxidative damage in experimental rats and the role of aqueous extract of Opuntia vulgaris fruit extract (OE) to counteract the toxicity induced by methanol. The animals were exposed to methanol at a dose of 2.37 g/kg body weight intraperitoneally for 30 days. OE was found to contain large amounts of polyphenols and carotenoids and significant antioxidant capacities highlighted by scavenging activities for 2,2-diphenyl-l-picrylhydrazyl. The treatment with methanol exhibited a significant increase in serum hepatic and renal biochemical parameters (alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, lactate dehydrogenase, bilirubin, urea, and creatinine). Methanol intoxication significantly increased hepatic and renal lipid peroxidation evaluated by thiobarbituric acid reactive substances in treated rats as compared to controls. However, hepatic and renal antioxidant enzymes namely superoxide dismutase, catalase, and glutathione peroxidase were significantly decreased in methanol-treated animals as compared to controls. The results concluded that treatment with OE prior to methanol intoxication has significant role in protecting animals from methanol-induced hepatic and renal histopathological and oxidative damage.     

Association between As and Cu renal cortex accumulation and physiological and histological alterations after chronic arsenic intake

Arsenic (As) is one of the most abundant hazards in the environment and it is a human carcinogen. Related to excretory functions, the kidneys in humans, animal models or naturally exposed fauna, are target organs for As accumulation and deleterious effects. Previous studies carried out using X-ray fluorescence spectrometry by synchrotron radiation (SR-μXRF) showed a high concentration of As in the renal cortex of chronically exposed rats, suggesting that this is a suitable model for studies on renal As accumulation. This accumulation was accompanied by a significant increase in copper (Cu) concentration. The present study focused on the localization of these elements in the renal cortex and their correlation with physiological and histological As-related renal effects. Experiments were performed on nine male Wistar rats, divided into three experimental groups. Two groups received 100 μg/ml sodium arsenite in drinking water for 60 and 120 consecutive days, respectively. The control group received water without sodium arsenite (<50 ppb As). For histological analysis, 5-μm-thick sections of kidneys were stained with hematoxylin and eosin. Biochemical analyses were used to determine concentrations of plasma urea and creatinine. The As and Cu mapping were carried out by SR-μXRF using a collimated white synchrotron spectrum (300 μm×300 μm) on kidney slices (2 mm thick) showing As and Cu co-distribution in the renal cortex. Then, renal cortical slices (100 μm thick) were scanned with a focused white synchrotron spectrum (30 μm×30 μm). Peri-glomerular accumulation of As and Cu at 60 and 120 days was found. The effects of 60 days of arsenic consumption were seen in a decreased Bowman's space as well as a decreased plasma blood urea nitrogen (BUN)/creatinine ratio. Major deleterious effects; however, were seen on tubules at 120 days of exposition. This study supports the hypothesis that tubular accumulation of As-Cu may have some bearing on the arsenic-associated nephrotoxicological process.     

BSO、GSH、VC和DMPS对汞肾毒性影响的实验研究

目的探讨一次染汞的肾脏毒性作用并观察2氨基4(S丁基磺酰亚氨)丁酸(BSO)、还原型谷胱甘肽(GSH)、维生素C(VC)和二巯基丙磺酸钠(DMPS)预处理对汞肾脏毒性的影响。方法Wistar大鼠64只,随机分成8组。第1组为对照组,第2～4组为低、中、高剂量染汞组,分别皮下注射0.75、1.5和2.5mg kg的氯化汞溶液,第5～8组为预处理干预组。BSO预处理组先腹腔注射BSO0.5mmol kgbw,4h后皮下注射0.75mg kgHgCl2溶液。其他3个预处理组中,先分别腹腔注射GSH3mmol kg,VC4mmol kg或DMPS200μmol kgbw,2h后皮下注射2.5mg kgHgCl2溶液。注射容量均为5ml kgbw。对照组皮下注射生理盐水。注射12h后收集大鼠12h尿液,采集血液,分离血清,切取肝脏和肾皮质样品。测定肝脏、肾皮质和尿中汞含量;尿NAG、ALP、LDH活性和尿蛋白,血清尿素氮(BUN)含量。结果染汞后肝、肾皮质和尿汞含量随染汞剂量加大而逐渐增加。肾皮质汞含量有明显的剂量-效应关系,高剂量组肝汞含量显著高于中低剂量组和对照组。中高剂量组尿汞含量显著高于对照组。BSO预处理组和单纯0.75mg kgHgCl2组比,使肝汞含量增加,肾皮质和尿汞含量降低。GSH、VC和DMPS预处理组肝汞含量显著低于单纯2.5mg kgHgCl2组。尿NAG、ALP、LDH活性和尿蛋白、BUN含量随染汞剂量加大而升高,且2.5mg kgHgCl2组显著高于对照组、0.75和1.5mg kg HgCl2组。BSO预处理组尿NAG、ALP活性和尿蛋白、BUN含量显著高于单纯0.75mg kgHgCl2组和对照组。GSH、VC和DMPS预处理组和单纯2.5mg kgHgCl2组相比,尿NAG、ALP、LDH活性和尿蛋白、BUN含量显著降低。结论随着染汞剂量增加,肝脏、肾皮质和尿汞含量也增加。BSO预处理可增强汞的肾脏毒性作用,而GSH、VC和DMPS预处理则对汞的肾脏毒性具有一定的拮抗作用。     

Effect of kidney damage on the mobilisation of mercury by thiol-complexing agents

ABSTRACT Mobilisation of mercury by thiol-complexing agents is the accepted treatment for chronic mercury intoxication. The success of such treatment is judged by the urinary excretion of mercury which might be modified by existing kidney damage caused either by the mercury itself or by other factors. In the present work the ability of three thiol-complexing agents, D-penicillamine, N-acetyl-D, L-penicillamine, and 2,3-dimercaptosuccinic acid (DMSA) to remove mercury from a damaged kidney and to increase the urinary excretion of mercury were studied. Kidney damage was induced by the injection of 20 mg/kg sodium chromate three days before the injection of 2·5 μmoles/kg HgCl₂ or three and seven days before the administration of a similar dose of mercury complexed with D-penicillamine.

It was shown that both renal uptake and urinary excretion of mercury were decreased in animals with damaged kidneys. This effect lessened with time between the induction of damage and the injection of mercury-penicillaminate.

Each of the three chelating agents was given 48 and 54 hours after the administration of HgCl₂ in equivalent (400 μmoles/kg) doses. All were able to remove mercury from the kidneys, but DMSA was far the most effective and only DMSA increased the urinary excretion of mercury. The amount of mercury removed from the kidneys by the chelators was less in animals with renal damage than in controls, but the difference was insignificant if renal mercury depletion was related to the initial renal mercury content.

     

Demethylation and excretion of methyl mercury by the guinea pig

Female guinea pigs were dosed po with 1.0 mg CH₃²⁰³Hg/kg as methylmercuric chloride, 10 times over a 3-week period. Tissue distribution, excretion, and accumulation of inorganic and organic mercury were studied. The highest concentration of mercury was found in the kidney. The greatest decreases of mercury levels were observed in the small bowel, red blood cells, liver, and cerebrum. The half-life of whole body clearance, based on a single compartment model, was 31.6 days. Mercury in the kidney, liver, and cerebrum was bound mainly by nuclear and soluble fractions. The highest ratio of inorganic to total mercury was seen in the kidney, 60% of this being as inorganic mercury. Excretion of mercury in the feces was measured throughout the experiment. The relationship of organic to inorganic mercury was relatively constant at about 1:3. Data on the effects of methyl mercury on tissue concentrations of zinc and copper show that the only change in the copper content was a marked increase in the kidney.     

Modifications in Rat Testicular Morphology and Increases in IFN-γ Serum Levels by the Oral Administration of Subtoxic Doses of Mercuric Chloride

Mercury induces structural and functional damage in several organs, however the effects of subtoxic doses of the metal on the male reproductive system are not well defined. In order to analyze testicular and epididymal morphological alterations and changes in IL-4 or IFN-γ serum levels, adult male Sprague-Dawley rats received 0.01, 0.05 or 0.1?μg/ml of mercuric chloride (HgCl₂) in deionized water for 1 to 7 months by oral route. Controls received deionized water alone. Twenty rats, separated in four groups of five animals each, were used per time of exposure. Progressive degenerative lesions consisting of lack of germ cell cohesion and desquamation, arrest at spermatocyte stage and hypospermatogenesis were observed in seminiferous epithelium by light and electron microscopy. Leydig cells showed cytoplasmic vacuolation and nuclear signs of cell death. Loss of peritubular cell aggregation was evidenced in the epididymis. Mercury accumulation was detected in both organs by mass spectroscopy. Rats showed enhanced IFN-γ serum levels as compared to controls but only reached significance after 7 months of mercury administration. Subtoxic doses of inorganic mercury could lead to reproductive and immunological alterations. The results demonstrate that sublethal concentrations of mercuric chloride are enough to induce morphological and ultrastructural modifications in male reproductive organs. These contribute to functional alterations of spermatogenesis with arrest at spermatocyte stage, hypospermatogenesis and possibly impaired steroidogenesis which together could affect male fertility.     

Effect of mercuric chloride and methylmercury chloride exposure on tissue concentrations of six essential minerals

There are few data on the effects of mercury exposure on tissue concentrations of essential minerals. Male Sprague-Dawley rats were exposed to mercuric chloride and methylmercury chloride administered via the drinking water. Subsequently, the kidneys, spleen, liver, and brain were analyzed for mercury, calcium, copper, magnesium, manganese, iron, and zinc by atomic absorption spectrophotometry. Significant differences from controls were found for brain copper, kidney copper, and kidney zinc in the mercuric chloride-exposed animals; and for brain iron, kidney copper, kidney iron, kidney magnesium, spleen magnesium, and liver manganese in the methylmercury chloride-exposed rats. There was a fivefold higher mean kidney copper concentration in the mercuric chloride-exposed group; this may be related to the induction of renal metallothionein synthesis by mercury. Increased kidney copper may be a manifestation of heavy metal-induced renal toxicity. Both inorganic and methylmercury exposure produce significant changes in tissue concentrations of some essential minerals.     

SD大鼠30d喂养试验血液学生化和脏器系数指标参考值探讨

目的探讨SD大鼠30d喂养试验血液学生化和脏器系数指标参考值。方法收集本实验室用于30d喂养试验的SD大鼠血液学生化和脏器系数指标进行分析。结果血液甘油三酯、尿素氮、肌酐、总蛋白含量及谷草转氨酶活性和肝体比及肾体比雌雄鼠间差异无显著性,谷丙转氨酶活性、血清白蛋白、血糖及总胆固醇含量和脾体比雌雄鼠间差异具有显著性;除雌性大鼠的脾脏系数(P=0.076)批间无差异外,其余各血液学生化和脏器系数指标分性别不同批次间比较差异具有显著性。结论血液学生化指标甘油三酯、尿素氮、肌酐、总蛋白含量及谷草转氨酶活性和脏器系数肝体比及肾体比雌雄鼠间可以合并。     

黄芩苷对雄性大鼠肝肾毒性作用研究

目的观察不同剂量黄芩苷给药不同时间对大鼠肝肾的毒性作用,为临床用药的安全性提供实验参考依据。方法于2019年4月,将42只Wistar雄性大鼠随机分为对照组(0.9%氯化钠溶液,14只)和黄芩苷给药组(100、200 mg/kg,各14只),经口灌胃,1次/d,6次/周,于给药28、56 d后各组分别处死7只大鼠,称量肝脏、肾脏湿重并计算脏器系数,采用苏木素-伊红(HE)染色检测其组织形态学改变,并检测大鼠血清中谷丙转氨酶(ALT)、谷草转氨酶(AST)、碱性磷酸酶(ALP)、尿素氮(BUN)和肌酐(CRE)的含量。结果黄芩苷200 mg/kg组大鼠给药56 d后体质量、肾脏系数均低于对照组(P<0.05),组织形态学显示肾小球萎缩变小、肾小管明显萎缩且上皮细胞发生坏死,肝脏未见明显异常。黄芩苷200 mg/kg组大鼠给药56 d后,血清中BUN、CRE含量高于对照组,差异均有统计学意义(P<0.05);黄芩苷100 mg/kg组各时间点和黄芩苷200 mg/kg组给药28 d后各指标均未见明显异常。结论在本试验条件下,黄芩苷给药对雄性大鼠有一定的肾脏毒性作用。     

Attenuation of renal ischemia-reperfusion injury by proanthocyanidin-rich extract from grape seeds

The effects of proanthocyanidin-rich extract in rats subjected to renal ischemia-reperfusion were examined. Proanthocyanidin-rich extract, which is prepared from grape seeds (Vitis vinifera L.), was given orally at doses of 5 and 10 mg/kg body weight/d for 20 consecutive days prior to ischemia-reperfusion. Administration of proanthocyanidin-rich extract attenuated renal dysfunction, as indicated by serum urea nitrogen and creatinine levels. Additionally, in the ischemic-reperfused kidneys, increased levels of thiobarbituric acid (TBA)-reactive substance and alterations of antioxidant enzyme activities such as superoxide dismutase, catalase and glutathione peroxidase (GSH-Px) were observed. Proanthocyanidin-rich extract-treated groups showed significantly reduced renal TBA-reactive substance levels and enhanced catalase and GSH-Px activities. These results suggest that proanthocyanidin-rich extract has protective effects against ischemia-reperfusion-induced renal damage associated with oxidative stress.     

七省(区)126所医疗机构水银体温计和水银血压计及其替代产品使用现状调查及相关建议

目的对七个省(区)126所医疗机构水银体温计和水银血压计及其相应的替代品使用现状进行调查,为制定《关于汞的水俣公约》履约政策提供参考。方法选择东部、中部、西部地区共七省(区)的三级医院、二级医院及乡镇卫生院共计126所医疗机构,调查2013—2016年水银体温计和水银血压计及其替代品使用情况。结果截至2016年3月1日,126所医疗机构正在使用的水银体温计数量156 088支,医疗机构使用率为100.00%,每床位使用量为0.11支;使用的水银血压计数量为13 576台,医疗机构使用率为100.00%,每床位使用量为0.010台。正在使用的无汞体温计数量10 510支,2013—2015年依次每年分别有40所(31.75%)、50所(39.68%)、52所(41.27%)医疗机构在使用。正在使用的无汞血压计数量为8 266台;2013—2015年依次每年分别有85所(67.46%)、83所(65.87%)、87所(69.05%)医疗机构在使用。结论部分医疗机构已经开始少量使用无汞体温计和无汞血压计;制定《关于汞的水俣公约》履约政策应注意提高使用无汞替代产品意识并提供政策及经费支持等。     

The mercury burden of the Czech population: An integrated approach

In this paper an integrated approach in assessment of the population exposure from various sources of total mercury (THg) oral intake in the Czech Republic is presented. The information on total mercury levels in diet, drinking water, surface urban soil and body fluids and tissues stem from the Czech national Environmental Health Monitoring System (EHMS) operated since 1994. The THg concentration was determined by the special atomic absorption spectrophotometer AMA 254. The data on THg content in food from the sales network were collected in 12 cities. The estimated average dietary intake representing more than 95% of weight of usual diet composition ranged 1–2% of the JECFA/FAO WHO provisional tolerable weekly intake (PTWI) value for total mercury (5 μg/kg b.w./week). Data on drinking water quality stem from the nationwide monitoring database. The content of THg in drinking water is generally low; only 0.2% of the Czech population supplied with drinking water from the distribution networks (total of 92% of the population) has a mercury intake from drinking water higher than 1% PTWI and not exceeding 5% PTWI. The estimation of potential mercury intake by unintentional consumption of soil in small children was based on THg content in surface soil of a total of 324 nursery schools in 24 cities and towns. Median value was 0.16 mg/kg. Human biomonitoring was performed in 9 Czech cities. In 2007, the mercury median values in blood of adults (N = 412) were 0.85 and 0.89 μg/l in males and in females, respectively; urine median value in adults was 1.10 μg/g creatinine. In 2008, the blood median value in children (N = 324) amounted to 0.35 μg/l; urine median value is 0.16 μg/g creatinine. In children's hair the median THg value was 0.18 μg/g. The correlation between fish consumption and blood THg levels was observed in both adults and children. Also the biomonitoring outputs did not reveal a substantial burden of the population.