Effect of Zinc on Cancerogenesis by Cadmium.

Gunn, Samuel A.; Gould, Thelma Clark; Anderson, Winston A.

doi:10.3181/00379727-115-28996

Cited by 88 publications

(34 citation statements)

References 2 publications

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“…Fourteen rats were observed for a period of one year but no neoplastic changes were reported. On the other hand, cadmium metal (Heath and Daniel, 1964), cadmium sulphate (Haddow et al, 1964;Gunn et al, 1964), cadmium sulphide and cadmium oxide have given rise to malignant tumours at the site of subcutaneous or intramuscular injection in the rat. In addition, interstitial cell tumours of the testis have followed subcutaneous injection of cadmium sulphate ).…”

Section: Discussionmentioning

confidence: 99%

“…Following this observation similar results were obtained in a group of rats given repeated injections of a soluble cadmium salt in the form of cadmium sulphate. (Haddow, Roe, Dukes and Mitchley, 1964;Roe, Dukes, Cameron, Pugh and Mitchley, 1964) Sarcomata at the injection site and testicular tumours were later reported following the single subcutaneous injection of a relatively small dose of cadmium chloride, another soluble compound (Gunn, Gould and Anderson, 1964). Finely divided cadmium metal suspended in serum and injected into the thigh muscle of the rat led to the production of rhabdomyosarcoma and fibrosarcoma in an experiment given in a preliminary report by Heath, Daniel, Dingle and Webb (1962), and described in detail by Heath and Daniel (1964).…”

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The induction of sarcoma in the rat by cadmium sulphide and by cadmium oxide.

Kazantzis¹,

Hanbury²

1966

Br J Cancer

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A NUMBER of metals and some of their compounds have shown evidence of carcinogenic activity in the experimental animal and a brief review of these agents has been given by Roe and Lancaster (1964). One metal currently receiving attention in this respect has been cadmium. The repeated subcutaneous injection of ferritin in a group of rats was found to produce malignant tumours at the injection site, testicular atrophy and interstitial cell tumours of the testis (Haddow, Dukes and Mitchley, 1]961). The ferritin had been prepared from rat-liver protein by precipitation with a cadmium salt. Following this observation similar results were obtained in a group of rats given repeated injections of a soluble cadmium salt in the form of cadmium sulphate. (Haddow, Roe, Dukes and Mitchley, 1964;Roe, Dukes, Cameron, Pugh and Mitchley, 1964) Sarcomata at the injection site and testicular tumours were later reported following the single subcutaneous injection of a relatively small dose of cadmium chloride, another soluble compound (Gunn, Gould and Anderson, 1964). Finely divided cadmium metal suspended in serum and injected into the thigh muscle of the rat led to the production of rhabdomyosarcoma and fibrosarcoma in an experiment given in a preliminary report by Heath, Daniel, Dingle and Webb (1962), and described in detail by Heath and Daniel (1964). The insoluble compound cadmium sulphide has also been shown to give rise to sarcomata at the site of subcutaneous injection in the rat (Kazantzis, 1963). The results of this experiment, performed independently in 1961, together with the findings in a further series, are now given in detail. The induction of sarcomata at the site of subcutaneous injection of cadmium sulphide was confirmed, and similar tumours were shown to follow intramuscular injection. However, the intratracheal instillation of cadmium sulphide was not followed by the development of tumours, although there were other pathological changes which will be reported separately. In a further experiment a high incidence of tumours was obtained at the injection site following the subcutaneous injection of a suspension of cadmium oxide. MATERIALS AND METHODWistar rats of the Chester Beatty strain were used. They were provided with water and with pellets of diet 41B (Medical Research Council) ad libitum. A standardised vitamin supplement was added, and the diet supplemented at intervals with liver, bread and milk. The animals were lightly anaesthetised with ether and the skin at the injection site was shaved and cleaned with spirit. A

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Section: Discussionmentioning

confidence: 99%

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The induction of sarcoma in the rat by cadmium sulphide and by cadmium oxide.

Kazantzis¹,

Hanbury²

1966

Br J Cancer

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“…Exposure of the workers to other pollutants may also influence carcinogenicity. For example, it has been shown that simultaneous subcutaneous injection of cadmium and zinc salts inhibits or prevents the carcinogenic effect on the testes and injection sites of cadmium chloride when administered alone (26,27). It is unknown whether this phenomenon would also be true for inhalational exposure.…”

Section: Extrapolation Of Pulmonary Effects Of Cadmium From Animals Tmentioning

confidence: 99%

Airborne cadmium and carcinogenesis of the respiratory tract.

Oberdörster¹

1986

Scand J Work Environ Health

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Airborne cadmium and carcinogenesis of the respiratory tract. by Oberdorster G This article in PubMed: www.ncbi.nlm.nih.gov/pubmed/3547632 J Work Environ Health 12 (1986) 523 -537 Airborne cadmium and carcinogenesis of the respiratory tract by Gunter Oberdorster, DrMedVet 1 OBERDORSTER G. Airborne cadmium and carci nogenesis of the respirat ory tract. Scand J Work En viron Health 12 (1986) 523-537. Exposure to airborne cadmium occurs mainly at the workplace. Significan t exposure also occurs through smoki ng. Results of a recent epidemiologic stu dy suggest that occupational inhalation of cadmium is connected with an increased lung cancer risk. This finding corrobo rates th e high lung cancer incidence found among rat s after chronic low-level exposure to cadmium chloride aero sols. Differences in the tumor sites, exposur e conditions, and the pulmonary metabolism of cadmium between rod ents and man mak e it diffi cult to extra polate quantitatively from rat s to humans. In contr ast to the workpl ace, concentrations of cadmium in ambient air ar e very low, a nd the risk of lung cancer is probably very low, even for people living close to cadm ium-emitting ind ustries . The chemical form of inhaled cadmium appears to be importa nt. While cadmium oxide and cadmium chloride seem to be equally toxic, cadmium sulfide exhibits a lower acute pulmonary toxicity. However, whether this is also true for carcinogenic effects is not known. Additional long-term inhalation studies with animal s and further evaluat ion of epidemiologic studie s are necessary to answer questions about the carcinogenic potency of cadmium compounds of different chemical form. As long as such results are not available, it is prudent to regard all cadmium compounds as having a carcinogenic potential. REVIEWS Scand

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“…Thus, protooncogene induction correlates with the metal specificity of the orphan receptor as well as reversible manipulation of orphan receptor responsiveness by varying the Zn2+ level of the culture medium. Notably Zn2+ markedly decreases tumor induction by Cd2+ (96)(97)(98). Further work is needed to evaluate the roles of protein phosphorylation and the putative orphan receptor in protooncogene induction and mitogenic stimulation by divalent metals.…”

Section: Protooncogene Induction By Cadmiummentioning

confidence: 99%

Transmembrane signals and protooncogene induction evoked by carcinogenic metals and prevented by zinc.

Smith

Smith²,

Pijuan³

et al. 1994

Environ Health Perspect

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Cd2+ provokes an immediate production of inositol trisphosphate and the release of Ca2+ from internal stores in human fibroblasts and some other mammalian cells. Ni2+, Co2+, Fe2+, and Mn2+ evoke the release of stored Ca2+, but are less potent than Cd2+ (apparent Ko05 = 40 nM). Zn2+ and Cu2+ competitively inhibit Ca2+ release evoked by Cd2, without affecting Ca2+ release by hormones such as bradykinin. Zn2+ has the same apparent Ki value (80-90 nM) towards the five agonist metals, which suggests that the metals interact with the same site. Many other divalent cations neither released stored Ca2+ nor affected Cd2+-evoked Ca2+ release. The agonist metals appear to activate phospholipase C via a G protein rather than a tyrosine kinase. The production of reactive oxygen species is probably not involved in Ca2+ release by the metals. Cd2+ and other stimuli that raise cytosolic-free Ca2+ induce cyclic (AMP) production, apparently by activating a calmodulin-dependent adenylyl cyclase. We suggest that an orphan receptor mediates the hormonelike responses to Cd2+ and the other agonist metals. The receptor is referred to as an orphan because its physiological stimulus is unknown. Growth of the fibroblasts in high Zn2+ desensitizes them to the five agonist metals without affecting Ca2+ release by bradykinin or histamine. A several hour incubation in culture medium with normal Zn2+ fully restores responsiveness to the five active metals. Growth in high Zn2+ appears to repress the synthesis of the putative orphan receptor because inhibitors of RNA or protein synthesis, or asparagine-linked glycosylation, prevented the restoration of metal responsiveness. Experiments with lectins and neuraminidase support the view that a cell surface sialoprotein mediates Cd2+ responsiveness. Cd2+ evokes rapid changes in 132P] incorporation by certain proteins, as would be expected for the activation of a phospholipase C-coupled receptor. Cd2+ and the other metals that trigger hormonelike messenger production, also induce protooncogenes. These observations have revealed a new target for certain metals which is extraordinary with respect to metal potency and specificity. Additionally, the work reviewed here supports the view that certain metals can promote cell growth, which results in part from the fortuitous induction of hormonelike signals. -Environ Health Perspect 102(Suppl 3): 181-189 (1994).

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Effect of Zinc on Cancerogenesis by Cadmium.

Cited by 88 publications

References 2 publications

The induction of sarcoma in the rat by cadmium sulphide and by cadmium oxide.

The induction of sarcoma in the rat by cadmium sulphide and by cadmium oxide.

Airborne cadmium and carcinogenesis of the respiratory tract.

Transmembrane signals and protooncogene induction evoked by carcinogenic metals and prevented by zinc.

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