Lymphocyte replicating ability in individuals exposed to arsenic via drinking water

Gonsebatt, María E.; Vega, Libia; Montero, Regina; Garcia-Vargas, Gonzalo; Razo, Luz M. Del; Albores, Arnulfo; Cebrián, Mariano E.; Ostrosky‐Wegman, Patricia

doi:10.1016/0165-1161(94)90059-0

Cited by 84 publications

(32 citation statements)

References 23 publications

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“…The decrease could suggest a slower progression of lymphocytes from S to M phase of the cell cycle. 49 No significant differences were observed in MI between asymptomatic and skin-symptomatic groups. CA was determined in 2 different ways, i.e., CA per cell and the percentages of aberrant cells.…”

Section: Ca In Lymphocytesmentioning

confidence: 80%

Cytogenetic damage and genetic variants in the individuals susceptible to arsenic‐induced cancer through drinking water

Ghosh

Basu

Mahata

et al. 2006

Intl Journal of Cancer

112

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In West Bengal, India, more than 300,000 arsenic-exposed people are showing symptoms of arsenic toxicity, which include cancers of skin and different internal organs. Since only 15-20% of the exposed population manifest arsenic-induced skin lesions, it is thought that genetic variation might play an important role in arsenic toxicity and carcinogenicity. A total of 422 unrelated arsenic-exposed subjects (244 skin-symptomatic and 178 asymptomatic) were recruited for this study. Cytogenetic damage, as measured by chromosomal aberrations in lymphocytes and micronuclei formation in oral mucosa cells, urothelial cells and binucleated lymphocytes, was studied in unexposed, skin-symptomatic and asymptomatic individuals with similar socioeconomic status. Identification of null mutations in GSTT1 and GSTM1 genes were carried out by PCR amplification. GSTP1 SNPs, implicated in susceptibility to various cancers, were assessed by PCR-RFLP method. Symptomatic individuals had higher level of cytogenetic damage compared to asymptomatic individuals and asymptomatic individuals had significantly higher genotoxicity than unexposed individuals. No difference in allelic variants in GSTT1 and GSTP1 was observed between these 2 groups. Incidence of GSTM1 null gene frequencies was significantly higher in the asymptomatic group. Individuals with GSTM1-positive (at least one allele) had significantly higher risk of arsenic-induced skin lesions (odds ratio, 1.73; 95% confidence interval, 1.24-2.22). These results show a protective role of GSTM1 null in arsenic toxicity. This study also indicates that asymptomatic individuals are sub clinically affected and are also significantly susceptible to arsenicinduced genotoxicity. ' 2005 Wiley-Liss, Inc.

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Section: Ca In Lymphocytesmentioning

confidence: 80%

Cytogenetic damage and genetic variants in the individuals susceptible to arsenic‐induced cancer through drinking water

Ghosh

Basu

Mahata

et al. 2006

Intl Journal of Cancer

112

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“…In a study of chronic exposure to another metal, arsenic (As), impairment of lymphocyte proliferation was observed in exposed individuals as compared to controls (Ostrosky-Wegman et al 1991, Gonsebatt et al 1994.…”

Section: Discussionmentioning

confidence: 99%

Cytogenetic damage related to low levels of methyl mercury contamination in the Brazilian Amazon

Amorim

Mergler

Bahia

et al. 2000

An. Acad. Bras. Ciênc.

104

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The mercury rejected in the water system, from mining operations and lixiviation of soils after deforestation, is considered to be the main contributors to the contamination of the ecosystem in the Amazon Basin. The objectives of the present study were to examine cytogenetic functions in peripheral lymphocytes within a population living on the banks of the Tapajós River with respect to methylmercury (MeHg) contamination, using hair mercury as a biological indicator of exposure. Our investigation shows a clear relation between methylmercury contamination and cytogenetic damage in lymphocytes at levels well below 50 micrograms/gram, the level at which initial clinical signs and symptoms of mercury poisoning occur. The first apparent biological effect with increasing MeHg hair level was the impairment of lymphocyte proliferation measured as mitotic index (MI). The relation between mercury concentration in hair and MI suggests that this parameter, an indicator of changes in lymphocytes and their ability to respond to culture conditions, may be an early marker of cytotoxicity and genotoxicity in humans and should be taken into account in the preliminary evaluation of the risks to populations exposed in vivo. This is the first report showing clear cytotoxic effects of long-term exposure to MeHg. Although the results strongly suggest that, under the conditions examined here, MeHg is both a spindle poison and a clastogen, the biological significance of these observations are as yet unknown. A long-term follow-up of these subjects should be undertaken.

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“…Although women appear to be better arsenic methylators than men, the relevance of this difference to arsenic-related health effects is unknown. Another example of a gender difference in the handling of arsenic comes from an in vitro study in the arsenical area of Mexico that found that impaired proliferation was greater in lymphocytes from arsenic-exposed women than from exposed men (35).…”

Section: Discussionmentioning

confidence: 99%

Methylation Study of a Population Environmentally Exposed to Arsenic in Drinking Water

Hopenhayn‐Rich¹,

Biggs²,

Smith³

et al. 1996

Environmental Health Perspectives

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Lymphocyte replicating ability in individuals exposed to arsenic via drinking water

Cited by 84 publications

References 23 publications

Cytogenetic damage and genetic variants in the individuals susceptible to arsenic‐induced cancer through drinking water

Cytogenetic damage and genetic variants in the individuals susceptible to arsenic‐induced cancer through drinking water

Cytogenetic damage related to low levels of methyl mercury contamination in the Brazilian Amazon

Methylation Study of a Population Environmentally Exposed to Arsenic in Drinking Water

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