Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (L6)
Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (L8, A18, A19, A28)
Evaluation: There is sufficient evidence in humans for the carcinogenicity of cadmium and cadmium compounds. There is sufficient evidence in experimental animals for the carcinogenicity of cadmium compounds. There is limited evidence in experimental animals for the carcinogenicity of cadmium metal. In making the overall evaluation, the Working Group took into consideration the evidence that ionic cadmium causes genotoxic effects in a variety of types of eukaryotic cells, including human cells. Overall evaluation: Cadmium and cadmium compounds are carcinogenic to humans (Group 1).
CLASSIFICATION: B1; probable human carcinogen. BASIS FOR CLASSIFICATION: Limited evidence from occupational epidemiologic studies of cadmium is consistent across investigators and study populations. There is sufficient evidence of carcinogenicity in rats and mice by inhalation and intramuscular and subcutaneous injection. Seven studies in rats and mice wherein cadmium salts (acetate, sulfate, chloride) were administered orally have shown no evidence of carcinogenic response. HUMAN CARCINOGENICITY DATA: Limited.
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌性证据
镉及其化合物:已知是人类致癌物。
Cadmium and Cadmium Compounds: known to be human carcinogens.
Evaluation: There is sufficient evidence in humans for the carcinogenicity of cadmium and cadmium compounds. There is sufficient evidence in experimental animals for the carcinogenicity of cadmium compounds. There is limited evidence in experimental animals for the carcinogenicity of cadmium metal. In making the overall evaluation, the Working Group took into consideration the evidence that ionic cadmium causes genotoxic effects in a variety of types of eukaryotic cells, including human cells. Overall evaluation: Cadmium and cadmium compounds are carcinogenic to humans (Group 1). /Cadmium and cadmium compounds/
To investigate the relationship between cadmium (Cd) toxicity, intestinal absorption, and its distribution to various tissues in rats treated orally with minimum amounts of Cd, 14 female rats per dose group per time point were given diets consisting of 28% purified diet and 72% ordinary rice containing Cd-polluted rice (0.02, 0.04, 0.12, or 1.01 ppm of Cd) or CdCl2 (5.08, 19.8, or 40.0 ppm of Cd) for up to 8 months. At 1, 4, and 8 months after the commencement of Cd treatment, seven rats per group were euthanized for pathological examinations to determine the Cd concentrations in the liver and kidneys and metallothionein (MT) in the liver, kidneys, intestinal mucosa, serum, and urine. One week before each period of 1, 4, and 8 months, the remaining seven rats in each group were administered a single dosage of Cd(109), a tracer, to match the amounts of the designated Cd doses (about 1.2 to 2400 ug/kg body wt). They were euthanized 5 days later to determine the distribution of Cd to various tissues. No Cd-related toxic changes were observed. The concentrations of Cd in the liver and kidneys at any time point and MT in the liver, kidney, serum, and urine at 4 and 8 months increased dose-dependently, whereas MT in the intestinal mucosa did not alter markedly at any time point. The distribution rates of Cd to the liver increased dose-dependently (40% at lower doses to 60% at higher doses), whereas those to the kidney decreased dose-dependently (20% at lower doses to 10% at higher doses). The Cd retention rates 5 days after Cd(109) administration (amounts of Cd in various tissues/amounts of Cd administered) ranged from 0.2 to 1.0% at any time point. These results suggest that the distribution of Cd to the liver and kidneys after the oral administration vary depending on the dosage levels of Cd. The difference of the distribution pattern of Cd to the liver and kidney is probably due to the difference in the form of the absorbed Cd, i.e., free ion or Cd-MT complex, although not closely related to the MT in the intestinal mucosa.
An increased body retention of Cd in rats orally pretreated with Cd or Zn is explained by induction of hepatic and renal metallothionein. Whether intestinal absorption of Cd increases after such treatments is not clear yet. To approach this problem we measured jejunal transfer rates of Cd(109) in vitro and in vivo in pretreated rats (0.44 mmol Cd/L or 4.6 mmol Zn/L in the drinking water for 10 days) and compared them with those of untreated controls. Isolated jejunal segments were used for in vitro perfusion. In vivo perfusion was performed in anaesthetized rats with blood collected from mesenteric venules substituting corresponding losses by reinfusion of rat blood. Water and glucose transfer did not differ between controls and pretreated rats. At a luminal concentration of 5 umol Cd(109)Cl2/L, Cd and Zn pretreatment significantly increased the transfer rate of Cd(109) in vitro and in vivo similarly. The Cd(109) transfer rates in controls in the final perfusion intervals (80-120 min) were 0.06 (pmol/cm/min) in vivo and 0.05 in vitro; the corresponding rates in Cd or Zn pretreated rats were significantly higher (P<0.05) and amounted to 0.11 and 0.18 or 0.15 and 0.23, respectively. Mucosal concentrations of Cd(109) measured at the end of the perfusion period tended to be lower in the pretreated animals than in the controls. This suggests that pretreatment with Cd or Zn reduces the amount of Cd(109) bound to the tissue leaving more Cd(109) for the transfer step. As compared to a level of mucosal metallothionein of 8 ug/g wet weight in controls, increased amounts of 67 or 52 ug/g wet weight in the Cd or Zn pretreated rats, respectively, thus did not decrease but increased transfer rates of Cd(109). Therefore, increased small intestinal transfer rates of Cd can contribute to increase the body retention of Cd seen after oral pretreatment with Cd or Zn.
ADULT RATS WERE INJECTED INTRAVENOUSLY WITH (109)CADMIUM CHLORIDE AND THE DISTRIBUTION OF THE ISOTOPE WITHIN THE BRAIN AND NEIGHBORING NERVOUS STRUCTURES WAS SUBSEQUENTLY STUDIED BY AUTORADIOGRAPHY. CADMIUM ACCUMULATED IN REGIONS OUTSIDE THE BLOOD-BRAIN BARRIER SUCH AS THE CHOROID PLEXUS, PINEAL GLAND AND AREA POSTREMA, BUT DID NOT APPEAR IN THE BRAIN PARENCHYMA. UPTAKE OF CADMIUM WAS OBSERVED IN THE TRIGEMINAL GANGLIA CLOSE TO THE NERVE CELLS AND IN THE OLFACTORY BULBS. IN ADDITION, CADMIUM ACCUMULATED IN THE IRIS, CILIARY BODY AND CHOROID OF THE EYE, BUT NOT IN THE OPTIC NERVES. THE DEPOSITION OF CADMIUM IN THE OLFACTORY BULBS MAY BE RELATED TO THE ANOSMIA REPORTED IN WORKERS EXPOSED TO THIS METAL.
CADMIUM CHLORIDE ADMIN TO RATS BY SC INJECTION OR DIRECTLY INTO LIVER IS TRANSPORTED TO TESTES. ... /ALSO, WHEN/ GIVEN SC TO RATS /IT/ APPEARED IMMEDIATELY IN PLASMA & THEN DISAPPEARED RAPIDLY; AFTER 6 DAYS ONLY 2% OF DOSE ... EXCRETED IN FECES.
Metal salt complexes of 3-isothiazolones and compositions containing them exhibit useful biocidal properties, including bactericidal, fungicidal, and algaecidal properties.
3-异噻唑酮的金属盐配合物及含有它们的组合物表现出有用的生物杀菌性能,包括杀菌、杀真菌和杀藻性能。
Metal salt complexes of 3-isothiazolones as effective biocidal agents
申请人:Rohm and Haas Company
公开号:US04396413A1
公开(公告)日:1983-08-02
Metal salt complexes of 3-isothiazolones and compositions containing them exhibit useful biocidal properties, including bactericidal, fungicidal, and algaecidal properties.
3-异硫氰酸盐金属配合物及含有它们的组合物表现出有用的杀菌特性,包括杀菌、杀真菌和杀藻特性。
Process for producing .alpha.-arylalkanoic acid ester
申请人:Taisho Pharmaceutical Company, Ltd.
公开号:US04433160A1
公开(公告)日:1984-02-21
A process for producing an .alpha.-arylalkanoic acid ester represented by the general formula ##STR1## wherein Ar represents an aryl group which may optionally be substituted, and R.sup.1 and R.sup.2, independently from each other, represent a lower alkyl group, which comprises reacting a Grignard reagent prepared from an aryl halide of the general formula Ar--X.sup.1 (II) wherein Ar is as defined above and X.sup.1 represents a halogen atom, and magnesium, with an .alpha.-haloalkanoic acid ester of the general formula ##STR2## wherein R.sup.1 and R.sup.2 are as defined above, and X.sup.2 represents a halogen atom, said reaction of the Grignard reagent with the .alpha.-haloalkanoic acid ester of general formula (III) being carried out in the presence of a nickel compound.
Fatty acids, soaps surfactant systems, and consumer products based thereon
申请人:——
公开号:US20040092418A1
公开(公告)日:2004-05-13
Novel fatty acids and derivatives thereof such as salts, new surfactant systems comprising one or more of these compounds, consumer products such as laundry products, personal care products, pharmaceutical compositions, industrial cleaners, and the like comprising said compounds or surfactant systems.
Fatty acids, soaps, surfactant systems, and consumer products based thereon
申请人:The Procter & Gamble Company
公开号:US20040092419A1
公开(公告)日:2004-05-13
Novel fatty acids and derivatives thereof such as salts, new surfactant systems comprising one or more of these compounds, consumer products such as laundry products, personal care products, pharmaceutical compositions, industrial cleaners, and the like comprising said compounds or surfactant systems.