Protective effect of selenium against arsenic-induced chromosomal damage in cultured human lymphocytes

Sweins, A.

doi:10.1111/j.1601-5223.1983.tb00602.x

Cited by 28 publications

(5 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Fifth, in some areas of the world, such as Bangladesh, the digging of tube wells has led to an epidemic of arsenic poisoning. Selenium is the natural antagonist of arsenic; when present they are both excreted in the bile as an insoluble complex [321][322][323][324][325][326][327]. High doses of selenium can be used to treat arsenic poisoning and vice versa.…”

Section: Seleniummentioning

confidence: 99%

Proposed Recommended Nutrient Densities for Moderately Malnourished Children

2009

View full text Add to dashboard Cite

Recommended Nutrient Intakes (RNIs) Key words: Ascorbate, biotin, calcium, catch-up growth, cobalamin, convalescence, copper, DRV, essential fatty acid, folic acid, growth, iodine, iron, magnesium, malnutrition, manganese, niacin, nutrient density, nutrition, nutritional deficiency, nutritional requirements, pantothenic acid, phosphorus, potassium, protein, protein-energy malnutrition, pyridoxine, RDA, recommendations, riboflavin, RNI, selenium, sodium, stunting, sulfur, thiamine, vitamin A, vitamin D, vitamin E, vitamin K, wasting, zinc SummaryThe objective is to derive nutrient requirements for moderately malnourished children that will allow them to have catch-up growth in weight and height, prevent their death from nutritional disease, strengthen their resistance to infection, allow for convalescence from prior illness, and promote normal mental, physical, and metabolic development.The malnourished population will have been exposed to nutritional stress and seasonal shortages and will have been living in unhygienic conditions; a proportion will have been severely malnourished. Typically, from 5% to 15% of children aged 6 to 59 months are moderately wasted, and 20% to 50% are stunted in height.There has been little published on the requirements for the moderately wasted or stunted child per se. However, with the change in definition of severe malnutrition from the Wellcome classification [1] based upon weight-for-age to one based upon weight-forheight, reanalysis of the data shows that many of the studies of children with less than 60% weight-for-age included children who were moderately wasted by modern criteria, albeit stunted. The physiological and other data from the older literature therefore are likely to apply to those with moderate as well as those with severe wasting.In order to derive the requirements of each nutrient for moderately malnourished children, the lower and upper boundaries were assumed to lie between the requirement for a normal, healthy child living in a clean environment and the requirement for treatment of a severely malnourished child living in a contaminated environment. The therapeutic diets used for treatment of the severely malnourished in the developing world have been remarkably successful and are capable of sustaining rates of weight gain of more than 10 g/kg/day and returning the children to physiological normality.The requirements for normal Western individuals (Recommended Nutrient Intake, RNI) were used as the minimum requirements. They were converted into nutrient:energy densities with the use of the energy

show abstract

Section: Seleniummentioning

confidence: 99%

Proposed Recommended Nutrient Densities for Moderately Malnourished Children

2009

View full text Add to dashboard Cite

show abstract

“…Selenium plays a special role in arsenic toxicity and susceptibility; the two metals show an antagonistic behavior in the body. Selenium was shown to have protective eŠects against arsenic-induced clastogenicity in cultured human lymphocytes (195). These results were further corroborated by a study on smelter workers exposed chronically to arsenic, where, the chromosomal aberration rate of cultured lymphocytes was lowered about 46.1z after treatment with selenium 150 g/d for 21 days (196).…”

Section: Role Of Diet In Arsenic Carcinogenicitymentioning

confidence: 76%

Arsenic-induced Cancers: A Review with Special Reference to Gene, Environment and Their Interaction

Banerjee

Bhattacharjee

Giri

2011

Genes and Environment

View full text Add to dashboard Cite

Chronic exposure to the toxic metalloid arsenic, either through occupational or environmental route results in the development of a plethora of dermatological as well as non-dermatological health eŠects, multi-organ cancers being the most severe ones. Several epidemiological studies have reported the occurrence of diŠerent types of cancers in populations exposed chronically to arsenic from diŠerent corners of the globe, but the spectrum of symptoms and severity vary widely. Several genetic and environmental factors might play an important causal role for such observed diŠerences, including genetic polymorphisms, dietary habits and socioeconomic status of the population. Unfortunately, the paradoxical nature of this carcinogen makes the use of animal model systems unsuitable, since they do not re‰ect the exact in vivo condition of arsenic exposure in human beings. Hence, in this present review, we have attempted to collate the isolated pieces of information available in existing literature depicting the various forms of arsenic-induced cancers, variations and etiology thereof. We have attempted to depict the entire spectrum of carcinogenic outcomes of chronic arsenic exposure and the interactions among several components like, genes (polymorphisms and mutations), environmental factors and dietary factors in the process. The literature reviews are primarily based on the human beings (in vivo), but to understand the underlying mechanism, we have also collated the information based on cell line models, and animal models where human data is scanty or unavailable. Thus, here we present a comprehensive review on the current state of research in theˆeld of arsenic-induced cancer and explore the underlying mechanism of arsenic-induced carcinogenicity, along with relevant historical perspective.

show abstract

“…There are several studies that suggest that inorganic arsenic may cause genotoxicity (mainly chromosomal effects) in exposed humans (Burgdorf et al 1977;Nordenson et al 1978), and this is supported by numerous studies in animals (Datta et al 1986;DeKnudt et al 1986;Nagymajtényi et al 1985) and cultured cells (Beckman and Nordenson 1986;Casto et al 1979;DiPaolo and Casto 1979;Lee et al 1985;Nakamuro and Sayato 1981;Nishioka 1975;Oberly et al 1982;Okui and Fujiwara 1986;Sweins 1983;Ulitzur and Barak 1988;Zanzoni and Jung 1980). The mechanism of genotoxicity is not known, but may be due to the ability of arsenite to interfere with DNA repair (Li and Rossman 1989) or to alter apoptosis (Pi et al 2005) or the ability of arsenate to act as a phosphate analog.…”

Section: Inorganic Arsenicalsmentioning

confidence: 90%

“…A number of researchers have found that arsenic compounds tend to reduce the effects of selenium (Hill 1975;Howell and Hill 1978;Kraus and Ganther 1989;Levander 1977;Miyazaki et al 2003;Moxon et al 1945;Schrauzer 1987;Schrauzer et al 1978). Likewise, selenium can decrease the effects of arsenic, including clastogenicity (Beckman and Nordenson 1986;Biswas et al 1999;Sweins 1983), delayed mutagenesis , cocarcinogenesis (Uddin et al 2005), cytotoxicity (Babich et al 1989;Rössner et al 1977;Styblo and Thomas 2001), and teratogenicity (Holmberg and Ferm 1969). The mechanism of this mutual inhibition of effects is not known, but may be related to the formation of a selenium-arsenic complex (seleno-bis [S-gluthionyl] arsinium ion; Gailer et al 2002) that is excreted more rapidly than either arsenic or selenium alone (Cikrt et al 1988;Hill 1975;Levander 1977;Levander and Baumann 1966) or due to selenium-induced changes in arsenic methylation (Styblo and Thomas 2001;Walton et al 2003).…”

Section: Interactions With Other Chemicalsmentioning

confidence: 99%