Release of corrosion products from amalgam in phosphate containing solutions

Abstract— The effect of phosphate concentration on corrosion was compared for two types of amalgam: a conventional alloy (ANA 68) and a high-Cu admixed alloy (Dispersalloy). The test specimens were stored for 4 months in electrolytes containing 85 mM NaCl and 85 mM NaCl with 2.5, 10, or 100 mM phosphate buffer respectively. The solutions were renewed each month and analyzed for Cu, Zn, Sn, Hg, and Ag in an atomic absorption spectrophotometer. The surfaces and cross-sections of the specimens were studied in a scanning electron microscope (SEM) with an energy dispersive detector (EDAX). The corrosion products, mainly Sn-compounds, at the surface of the amalgams were less in the solutions containing high concentrations of phosphate. In cross-section subsurface corrosion of the high-Cu amalgam was observed especially in specimens immersed in the NaCl solution without phosphate. The conventional amalgam showed surface corrosion only. The decrease in release of elements with time from the conventional amalgam in all the experimental solutions might indicate passivation. For the high-Cu amalgam the release of elements increased with time, except for Cu and Sn in the solution with 100 mM phosphate, indicating that phosphate inhibits corrosion of the Cu-Sn-phases. Release of corrosion products from the high-Cu amalgam was more dependent on the presence of phosphate than the conventional amalgam.     

Immune modulation by cadmium and lead in the acute reporter antigen-popliteal lymph node assay.

Immune modulation by heavy metals may cause serious adverse health effects in humans, although the mechanisms involved are not well understood. Both cadmium and lead are important environmental and occupational toxins. Therefore, in the current study, the costimulatory/adjuvant effects and the T-cell-activating potential of these metals (i.e., CdCl2 and PbCl2), are examined. These immune-modulating properties are critical in the development of conditions such as allergy, hypersensitivity, and autoimmunity. Using the direct popliteal lymph node assay (PLNA) and reporter antigen-popliteal lymph node assay (RA-PLNA) both metals were examined individually for immunotoxicity. Mercury (i.e., HgCl2) was included for comparative purposes as its effects in the RA-PLNA are well documented. Seven days following a single footpad injection containing metal and/or RA (trinitrophenyl-ovalbumin [TNP-OVA] or TNP-Ficoll), BALB/c mice were sacrificed and the popliteal lymph nodes (PLNs) removed. PLN cellularity, TNP-specific antibody-secreting cells (ASCs), and lymphocyte subsets were assessed. All three metals strongly stimulated T- and B-cell proliferation and ASC production following coinjection with the RA TNP-OVA. In each case, ASC production was skewed towards the IgG1 isotype. In addition, all three metals induced IgG production to TNP-Ficoll (although relatively weakly in the case of Cd). These results show that each of these metals can provide adjuvant signals to promote lymphocyte proliferation and enhance adaptive immune responses to unrelated antigens. Skewing of immune responses towards T helper type 2 responses suggests that each of these metals can enhance allergic and hypersensitivity reactions to environmental antigens. Furthermore, the induction of IgG responses to TNP-Ficoll, a T-cell-independent antigen, indicates that each of these metals can activate neoantigen-specific T cells. T-cell activation by metals can lead to metal hypersensitivity and has been implicated in the development of autoimmunity. This is the first report of immune modulation by CdCl2 and PbCl2 in the RA-PLNA.     

Assessment of metallothionein and antibodies to metallothionein in normal and autistic children having exposure to vaccine-derived thimerosal

Allergic autoimmune reaction after exposure to heavy metals such as mercury may play a causal role in autism, a developmental disorder of the central nervous system. As metallothionein (MT) is the primary metal-detoxifying protein in the body, we conducted a study of the MT protein and antibodies to metallothionein (anti-MT) in normal and autistic children whose exposure to mercury was only from thimerosal-containing vaccines. Laboratory analysis by immunoassays revealed that the serum level of MT did not significantly differ between normal and autistic children. Furthermore, autistic children harboured normal levels of anti-MT, including antibodies to isoform MT-I (anti-MT-I) and MT-II (anti-MT-II), without any significant difference between normal and autistic children. Our findings indicate that because autistic children have a normal profile of MT and anti-MT, the mercury-induced autoimmunity to MT may not be implicated in the pathogenesis of autism.     

An analysis of the paradoxical effect of morphine on runway speed and food consumption

A previously reported paradigm in which rats run down a runway for food reward followed by morphine injection was analyzed to assess the utility of the paradigm in studies of opiate reinforcement. One experiment replicated the original report that post-trial morphine caused both an increase in runway speed and a decrease in food consumption (taste aversion) over successive trials, and showed in addition that the increase in runway speed did not occur as a result of food deprivation alone, but required the animals to have consumed food in the goal box. A second study using the quaternary opiate antagonist methyl naltrexone to block the peripheral effects of morphine suggested that the increase in runway speed has a peripheral locus while the taste aversion has a central one. A third experiment in which morphine was microinjected into either the lateral ventricle or the ventral tegmental area supported these observations, in that intracranial morphine failed to result in an increased runway speed, but did produce taste aversion after microinjection into either site. These findings also suggest that the increase in runway speed caused by post-trial morphine in this experiment has a peripheral locus of effect, which is probably distinct from the central effect that supports morphine self-administration and conditioned place preference. Offprint requests to: W.A.CorrigallThe views expressed in this publication are those of the authors and do not necessarily reflect those of the Addiction Research Foundation     

松花江同江江段渔民发汞值调查

本文对松花江同江江段沿江渔民于1990年4月进行头发总汞值调查。调查结果,渔民发汞值中位数为2.574ppm。处于受汞污染状态,即4ppm以上者仅占24.46％。没有超过10ppm者。     

松花江汞污染治理后沿江渔民发汞调查

调查结果表明，沿江渔民发汞均值为２．２５μｇ／ｇ，与对照点相比差异显著（Ｐ＜０．０１），其中扶余一松江段渔民发汞均值２．５４μｇ／ｇ，高于其他各江段；３０～４０岁年龄组渔民发汞值超过正常值者占４５％，比其他各年龄组多；在调查的１１９５人中有２５名发汞值超过１０μｇ／ｇ，其中１８人发甲基汞含量超过５μｇ／ｇ。     

汞对人体必需元素干扰的研究

对42例汞吸收、2例汞中毒者(尿汞>99.7nmol/L),采用原子吸收光谱法,检测了汞对人体必需五种金属元素代谢的干扰。研究发现,汞时人体必需元素镁、铜具有拮抗作用。汞吸收者血清镁极显著低于对照组(P>0.01)。经驱汞治疗后,血清镁、铜自然上升与对照组无统计学差异(P>0.05),镁离子低下,可出现神经肌纤维兴奋性增高。由此推测,汞引起肌肉震颤的毒理,可能由汞拮抗镁离子低下引起。设想,对汞中毒者采用补镁制剂治疗,是否具有驱汞作用值得探讨。     

接触金属汞的工人淋巴细胞微核率和姊妹染色单体互换率的观察

用机械法可使菜籽粕中毒性质的丙基异硫氰酸酯由０．７１％降到０．２１％，脱除率为７０．４２％，可替代猪、鸡中部分豆饼、鱼粉、降低饲料成本９．５６％－１２．６９％，县地生产性能不良影响。这种脱毒菜籽粕在体重３５－６０ｋｇ阶段猪日粮中用量不宜超过２０％；在肉仔鸡日糖中用量可为１０％或１５％。     

小剂量氯化汞对小鼠脂质过氧化物的影响

本观察小剂量１ｍｇ／ｋｇ）ＨｇＣｌ２对小鼠肝，脑组织中脂质过氧化物（ＬＰＯ）的影响，发现小剂量ＨｇＣｌ２可使肝组织中ＬＰＯ含量明显增高，与对照组比，差异有显性（Ｐ〈０．０２５），而脑组织中ＬＰＯ含量未见明显影响（Ｐ〉０．０５）。     

Chronic administration of theophylline to rats induces a post-insulin binding defect in adipocyte glucose transport

Summary To determine whether adenosine is involved in long-term regulation of glucose transport in adipose tissue, we have investigated effects of administration of an adenosine receptor antagonist (theophylline) on adipocyte glucose transport. Rats were injected with theophylline (30 mg/kg, dissolved in 0.9% NaCl) daily for 7 days. Controls were injected with saline. The rats were then killed, and epididymal adipocytes were isolated. Insulin-stimulated glucose transport rates were decreased by about 25%–30% in the cells from theophylline-treated rats at all insulin concentrations tested. The half-maximally effective concentration of insulin was not altered (6.5±0.5 and 6.7±0.5 mU/l in control and treated cells respectively), suggesting a post-insulin binding defect. This was confirmed by the finding that ¹²⁵I-insulin binding to the cells was not altered. Adenosine receptor number and affinity (measured on detergent-solubilized adipocyte extracts using ¹²⁵I-hydroxyphenylisopropyl adenosine) was also not changed by theophylline treatment. We conclude that theophylline administration causes decreased glucose transport rates in rat adipocytes at a post-insulin binding level. Thus, chronic adenosine receptor blockade impairs adipocyte glucose transport, suggesting that adenosine is involved in long-term regulation of glucose metabolism in adipose tissue.