The toxicity of an organic arsenical, 3-nitro-4-hydroxyphenylarsonic acid

Prier, R. F.; Nees, P. O.; Derse, P. H.

doi:10.1016/0041-008x(63)90024-3

Cited by 15 publications

(12 citation statements)

References 3 publications

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“…Organic arsenic compunds such as carbarsone (80,81), arsanilic acid (66, 82) and 3-nitro-4-hydroxyphenylarsonic acid (83) have been tested for carcinogenicity. The exposure routes included peroral administration, skin application or subcutaneous injection.…”

Section: Experimental Studiesmentioning

confidence: 99%

The carcinogenicity of arsenic.

Pershagen¹

1981

Environ Health Perspect

138

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A carcinogenic role of inorganic arsenic has been suspected for nearly a century. Exposure to inorganic arsenic compounds occurs in some occupational groups, e.g., among smelter workers and workers engaged in the production and use of arsenic containing pesticides. Substantial exposure can also result from drinking water in certain areas and the use of some drugs. Tobacco and wine have had high As concentrations due to the use of arsenic containing pesticides.Inorganic arsenic compounds interfere with DNA repair mechanisms and an increased frequency of chromosomal aberrations have been observed among exposed workers and patients.Epidemiological data show that inorganic arsenic exposure can cause cancer of the lung and skin. The evidence of an etiologic role of arsenic for angiosarcoma of the liver is highly suggestive; however, the association between arsenic and cancer of other sites needs further investigation. No epidemiological data are available on exposure to organic arsenic compounds and cancer. Animal carcinogenicity studies involving exposure to various inorganic and organic arsenic compounds by different routes have been negative, with the possible exception of some preliminary data regarding lung cancer and leukemia. Some studies have indicated an increased mortality from lung cancer in populations living near point emission sources of arsenic into the air. The role of arsenic cannot be evaluated due to lack of exposure data.Epidemiological data suggest that the present WHO standard for drinking water (50 ,g As/l.) provides only a small safety margin with regard to skin cancer.

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Section: Experimental Studiesmentioning

confidence: 99%

The carcinogenicity of arsenic.

Pershagen¹

1981

Environ Health Perspect

138

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“…Kanisawa and Schroeder did report that 19 of 91 rats fed arsenic developed unspecified pretumorous liver lesions, whereas such lesions were seen in only 10 of 82 controls. Prier et al (1963) Kroes et al (1974) failed to induce neoplasms or to demonstrate any synergistic effect with diethylnitrosamine by feeding specific-pathogen-freederived Wistar rats with lead arsenate or sodium arsenate at dietary levels of 1,850 and 463 ppm, respectively.…”

Section: Micementioning

confidence: 91%

“…Subcutaneous injection into 100 Swiss mice of 3N 4 HPA (total dose in females, 10 mg; in males, 5 mg) induced no tumors at the injection site or elsewhere after 2 yr of treatment (Prier et al, 1963).…”

Section: Subcutaneous and Intramuscular Administrationmentioning

confidence: 99%

“…Although there was an untreated control group, Sanderson did not run either carcinogen-treated or croton oil-treated controls, making interpretation of his results difficult. Prier et al (1963) Hueper and Payne (1962) found no more tumors in treated animals than in controls, when 50 C57BL mice were fed arsenic trioxide in drinking water (0.0004% of a 12% aqueous ethanol solution) for 15 months.…”

Section: Introductionmentioning

confidence: 98%

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Arsenic and cancer: The still unanswered question

Pelfrène¹

1976

Journal of Toxicology and Environmental Health

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For some 2,500 years, arsenic was considered an important element of pharmacopeias and was praised for its medicinal qualities. However, an incidental link with cancer was suggested during the nineteenth century, and since that time a controversy has ensued with regard to the compound's tumorigenicity. Several epidemiological surveys, for example, have suggested that arsenic induces lung, liver, or skin cancer in humans. On the other hand, all experimental attempts to reproduce such neoplasms in laboratory animals have consistently failed, thereby denying support to the human data. Recently arsenic was reported to be mutagenic. However, because of the inconsistency of most mutagenesis findings at present, this also cannot be regarded as supporting evidence. Furthermore, a recent trend has been to consider arsenic as beneficial in cancer prevention and in maintaining the health of farm animals, and, perhaps, humans. A critical review of epidemiological and experimental data from the literature has been made in an attempt to present an objective picture of this controversial and sensitive question and to encourage further research, which may ultimately determine whether arsenic deserves its execrable reputation.

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“…Roxarsone (3-nitro-4-hydroxyphenylarsonic acid) has been commonly used as a growth promotant in both swine and poultry. The toxic effects of roxarsone have been studied in several species with the emphasis placed primarily on poultry, rats and turkeys (Kerr et al, 1963;Prier et al, 1963;Sullivan and AI-Timimi, 1972;Wise et al, 1974;Rice et al, 1980;Czamecki et al, 1984).…”

Section: Introductionmentioning

confidence: 99%

Toxic Effects of Supplemental Copper and Roxarsone When Fed Alone or in Combination to Young Pigs

Edmonds

Baker

1986

Journal of Animal Science

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Three experiments were conducted to investigate the roxarsone (3-nitro-4-hydroxyphenylarsonic acid) X copper (Cu) interaction in weanling pigs. Supplemental roxarsone at 400 mg/kg diet decreased rate and efficiency of weight gain and caused visible neurological signs of toxicosis. Copper addition (CuSO4 X 5H2O) at a level of 650 mg Cu/kg diet likewise decreased weight gain and feed efficiency, and it also increased hepatic Cu deposition. The combination of these growth-depressing dosages of roxarsone and Cu resulted in a far greater reduction in gain and efficiency of feed utilization than was the case when either compound was fed alone. A growth-promoting dosage of Cu (250 mg/kg) increased weight gain by 32% in one experiment but showed no efficacy in alleviating the growth-depression resulting from feeding 400 mg/kg roxarsone. A roxarsone dosage of 100 mg/kg increased gain and feed efficiency. Surprisingly, the decreased weight gain in pigs fed 650 mg/kg Cu was ameliorated by feeding 100 mg/kg roxarsone concomitantly. This level of roxarsone also reduced liver Cu concentration substantially. It thus appears that the nature of the roxarsone X Cu interaction is dependent on the dose of each compound administered. Moreover, low-dose roxarsone administration appears to ameliorate Cu toxicity, but low-dose Cu feeding does not show efficacy against roxarsone toxicity.

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The toxicity of an organic arsenical, 3-nitro-4-hydroxyphenylarsonic acid

Cited by 15 publications

References 3 publications

The carcinogenicity of arsenic.

The carcinogenicity of arsenic.

Arsenic and cancer: The still unanswered question

Toxic Effects of Supplemental Copper and Roxarsone When Fed Alone or in Combination to Young Pigs

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