Exposure to arsenic in utero is associated with various types of DNA damage and micronuclei in newborns: a birth cohort study

Navasumrit, Panida; Chaisatra, Krittinee; Promvijit, Jeerawan; Parnlob, Varabhorn; Waraprasit, Somchamai; Chompoobut, Chalida; Binh, Ta Thi; Hai, Doan Ngoc; Bao, Nguyen Duy; Hai, Nguyen Khac; Kim, Kyoung-Woong; Samson, Leona D.; Graziano, Joseph H.; Mahidol, Chulabhorn; Ruchirawat, Mathuros

doi:10.1186/s12940-019-0481-7

Cited by 36 publications

(26 citation statements)

References 51 publications

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“…We used a combination of genetic and pharmacological approaches to demonstrate in vivo that oxidative stress is the initiating cause of arsenic poisoning in a tissue specific manner [54]. The absence of murine p21 induction is interesting in the light of the evidence that iAs exposure has the capacity to induce DNA damage in exposed infants [44].…”

Section: Discussionmentioning

confidence: 99%

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Application of the in vivo oxidative stress reporter Hmox1 as mechanistic biomarker of arsenic toxicity

Iñesta-Vaquera

Navasumrit

Henderson

et al. 2021

Environmental Pollution

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Section: Discussionmentioning

confidence: 99%

“…Epidemiological studies have linked arsenic exposure in utero and in adults to oxidative DNA damage [10,44]. This can result in toxicity by apoptosis mediated by the p53 pathway [45][46][47].…”

Section: Effect Of Arsenic Exposure On Ho-1 and P21 Reporter Expressionmentioning

confidence: 99%

Application of the in vivo oxidative stress reporter Hmox1 as mechanistic biomarker of arsenic toxicity

Iñesta-Vaquera

Navasumrit

Henderson

et al. 2021

Environmental Pollution

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“…The results also suggested that increased exposure to iAs alters the proportion of metabolites in urine. 9,24,36,37 Arsenic exposure linked to changes in gene expression patterns in cells or populations. 17,19,20,38 Studies had shown that iAs could change the expression of apoptosis-related genes.…”

Section: Discussionmentioning

confidence: 99%

The ability of arsenic metabolism affected the expression of lncRNA PANDAR, DNA damage, or DNA methylation in peripheral blood lymphocytes of laborers

Zhang

Chen

et al. 2019

Hum Exp Toxicol

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Arsenic has been associated with significant effects on human health. Exposure to inorganic arsenic has been associated with the changes in gene expression. Promoter of CDKN1A antisense DNA damage activated RNA (PANDAR) expression is induced by p53 protein and DNA damage response. Here, we investigated whether the ability of arsenic metabolism in individuals affected the expression of PANDAR, DNA damage, and DNA methylation. Levels of gene expression and DNA damage were examined by the quantitative polymerase chain reaction and DNA methylation was measured by the methylation-sensitive high-resolution melting curve. In our study, we demonstrated that arsenic exposure increased PANDAR expression and DNA damage among arsenic smelting plant laborers. The PANDAR expression and DNA damage were positively linked to monomethylarsonic acid % ( R = 0.25, p < 0.05 and R = 0.32, p < 0.01) and negatively linked to dimethylarsinic acid % ( R = −0.21, p < 0.05 and R = −0.31, p < 0.01). Subjects with low primary methylation index had increased levels of DNA damage (51.62 ± 2.96 vs. 60.93 ± 3.10, p < 0.05) and methylation (17.14 (15.88–18.51) vs. 15.83 (14.82–18.00), p < 0.05). Subjects with low secondary methylation index had increased levels of PANDAR expression (4.88 ± 0.29 vs. 4.07 ± 0.23, p < 0.01) and DNA damage (17.38 (15.88–19.29) vs. 15.83 (14.82–17.26), p < 0.01). DNA methylation of PANDAR gene was linked to the regulation of its expression in peripheral blood lymphocytes among laborers ( Y = −2.08 × X + 5.64, p < 0.05). These findings suggested arsenic metabolism ability and exposure affected the expression of PANDAR, DNA damage, and DNA methylation.

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“…First, 8-Hydroxy-2-deoxyguanosine (8-OHdG), a form of reactive oxygen species (ROS) and a major form of oxidative DNA damage, was obtained from urine and skin tissue of arsenic exposed individuals [27]. Early genetic effects including DNA strand breaks, micronuclei in cord blood, and nitrative DNA damage were found in arsenic exposed patients [28]. In addition, oxidative damages and mitochondrial mutations might play a role in arsenic-induced skin malignancies [29,30].…”

Section: Pathophysiological Mechanisms Of Arsenic-induced Carcinogmentioning

confidence: 99%

Arsenic-Induced Carcinogenesis and Immune Dysregulation

Huang

Lee

2019

IJERPH

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Arsenic, a metal ubiquitously distributed in the environment, remains an important global health threat. Drinking arsenic-contaminated water is the major route of human exposure. Exposure to arsenic contributes to several malignancies, in the integumentary, respiratory, hepatobiliary, and urinary systems. Cutaneous lesions are important manifestations after long-term arsenic exposure. Arsenical skin cancers usually herald the development of other internal cancers, making the arsenic-induced skin carcinogenesis a good model to investigate the progression of chemical carcinogenesis. In fact, only a portion of arsenic-exposed humans eventually develop malignancies, likely attributed to the arsenic-impaired immunity in susceptible individuals. Currently, the exact pathophysiology of arsenic-induced carcinogenesis remains elusive, although increased reactive oxidative species, aberrant immune regulations, and chromosome abnormalities with uncontrolled cell growth might be involved. This review discusses how arsenic induces carcinogenesis, and how the dysregulated innate and adaptive immunities in systemic circulation and in the target organs contribute to arsenic carcinogenesis. These findings offer evidence for illustrating the mechanism of arsenic-related immune dysregulation in the progression of carcinogenesis, and this may help explain the nature of multiple and recurrent clinical lesions in arsenic-induced skin cancers.

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Exposure to arsenic in utero is associated with various types of DNA damage and micronuclei in newborns: a birth cohort study

Cited by 36 publications

References 51 publications

Application of the in vivo oxidative stress reporter Hmox1 as mechanistic biomarker of arsenic toxicity

Application of the in vivo oxidative stress reporter Hmox1 as mechanistic biomarker of arsenic toxicity

The ability of arsenic metabolism affected the expression of lncRNA PANDAR, DNA damage, or DNA methylation in peripheral blood lymphocytes of laborers

Arsenic-Induced Carcinogenesis and Immune Dysregulation

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