Oxidative DNA damage of peripheral blood polymorphonuclear leukocytes, selectively induced by chronic arsenic exposure, is associated with extent of arsenic-related skin lesions

Pei, Qiu-ling; Ma, Ning; Zhang, Jing; Xu, Wenchao; Li, Yong; Ma, Zhifeng; Li, Yunyun; Tian, Fengjie; Zhang, Wenping; Mu, Jin-jun; Li, Yuanfei; Wang, Dongxing; Liu, Haifang; M, Yang; Ma, Caifeng; Yun, Fen

doi:10.1016/j.taap.2012.10.031

Cited by 26 publications

(11 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Oxidative damage, which is a reliable result of chronic arsenic exposure, can be predicted by neutrophilic DNA damage. It has been proposed as a measure of arsenicosis in exposed populations [59]. …”

Section: Arsenic Toxicitymentioning

confidence: 99%

The mechanistic basis of arsenicosis: Pathogenesis of skin cancer

et al. 2014

View full text Add to dashboard Cite

Significant amounts of arsenic have been found in the groundwater of many countries including Argentina, Bangladesh, Chile, China, India, Mexico, and the United States with an estimated 200 million people at risk of toxic exposure. Although chronic arsenic poisoning damages many organ systems, it usually first presents in the skin with manifestations including hyperpigmentation, hyperkeratoses, Bowen’s disease, squamous cell carcinoma, and basal cell carcinoma. Arsenic promotes oxidative stress by upregulating nicotinamide adenine dinucleotide phosphate oxidase, uncoupling nitric oxide synthase, and by depleting natural antioxidants such as nitric oxide and glutathione in addition to targeting other proteins responsible for the maintenance of redox homeostasis. It causes immune dysfunction and tissue inflammatory responses, which may involve activation of the unfolded protein response signaling pathway. In addition, the dysregulation of other molecular targets such as nuclear factor kappa B, Hippo signaling protein Yap, and the mineral dust-induced proto-oncogene may orchestrate the pathogenesis of arsenic-mediated health effects. The metalloid decreases expression of tumor suppressor molecules and increases expression of pro-inflammatory mitogen-activated protein kinase pathways leading to a tumor-promoting tissue microenvironment. Cooperation of upregulated signal transduction molecules with DNA damage may abrogate apoptosis, promote proliferation, and enhance cell survival. Genomic instability via direct DNA damage and weakening of several cellular DNA repair mechanisms could also be important cancer development mechanisms in arsenic-exposed populations. Thus, arsenic mediates its toxicity by generating oxidative stress, causing immune dysfunction, promoting genotoxicity, hampering DNA repair, and disrupting signal transduction, which may explain the complex disease manifestations seen in arsenicosis.

show abstract

Section: Arsenic Toxicitymentioning

confidence: 99%

The mechanistic basis of arsenicosis: Pathogenesis of skin cancer

et al. 2014

View full text Add to dashboard Cite

show abstract

“…Moreover, the arsenic-induced ROS generation has been related with alteration of signaling pathways inside the cells and transcription factors regulation, which are two mechanisms that play a crucial role in carcinogenesis [9]. In particular, a very recent study has observed that chronic exposure of humans to low levels of arsenic selectively induces oxidative DNA damage of peripheral blood polymorphonuclear cells, increasing and accelerating apoptosis of these cells [10]. Furthermore, interestingly, prenatal arsenic exposure has been associated with oxidative stress in cord blood and with a reduced thymic function, suggesting subsequent immunosuppression in childhood [11].…”

Section: Introductionmentioning

confidence: 99%

Arsenic-Induced Genotoxicity and Genetic Susceptibility to Arsenic-Related Pathologies

Faita

Cori

Bianchi

et al. 2013

IJERPH

114

View full text Add to dashboard Cite

The arsenic (As) exposure represents an important problem in many parts of the World. Indeed, it is estimated that over 100 million individuals are exposed to arsenic, mainly through a contamination of groundwaters. Chronic exposure to As is associated with adverse effects on human health such as cancers, cardiovascular diseases, neurological diseases and the rate of morbidity and mortality in populations exposed is alarming. The purpose of this review is to summarize the genotoxic effects of As in the cells as well as to discuss the importance of signaling and repair of arsenic-induced DNA damage. The current knowledge of specific polymorphisms in candidate genes that confer susceptibility to arsenic exposure is also reviewed. We also discuss the perspectives offered by the determination of biological markers of early effect on health, incorporating genetic polymorphisms, with biomarkers for exposure to better evaluate exposure-response clinical relationships as well as to develop novel preventative strategies for arsenic- health effects.

show abstract

“…To name a few, other neutrophil-related dermatosis are arsenic-induced skin lesions (Pei et al, 2013), pemphigus vulgaris (Yesilova et al, 2013), and psoriasis (Rocha-Pereira et al, 2004). Importantly, the overproduction of ROS by activated neutrophils may cause damage in skin proteins, lipids, and DNA.…”

Section: Resultsmentioning

confidence: 99%

Stem bark and flower extracts ofVismia caulifloraare highly effective antioxidants to human blood cells by preventing oxidative burst in neutrophils and oxidative damage in erythrocytes

Ribeiro

Berto

Ribeiro

et al. 2015

Pharmaceutical Biology

View full text Add to dashboard Cite

(2015) Stem bark and flower extracts of Vismiacauliflora are highly effective antioxidants to human blood cells by preventing oxidative burst in neutrophils and oxidative damage in erythrocytes, Pharmaceutical Biology, 53:11, 1691-1698, DOI: 10.3109/13880209.2014 Previous research on V. cauliflora extracts suggests its potential to neutralize cellular oxidative damages related to the production of reactive oxygen and nitrogen species.Objective: To determine the activity of stem bark and flower extracts of V. cauliflora on the modulation of oxidative burst in human neutrophils, as well as its potential to inhibit oxidative damage in human erythrocytes. Materials and methods:The modulation of neutrophil's oxidative burst by the ethanolic extracts (0.3-1000 mg/mL) was determined by the oxidation of specific probes by reactive species. Additionally, the potential of these extracts to inhibit oxidative damage in human erythrocytes was evaluated by monitoring its biomarkers of oxidative stress. Results: Vismia cauliflora extracts presented remarkable capacity to prevent the oxidative burst in activated human neutrophils (IC 50 515 mg/mL). However, the maximum percentage of inhibition achieved against hydrogen peroxide was 45%. Concerning the oxidative damage in human erythrocytes, the extracts were able to minimize the tert-butyl hydroperoxide-induced hemoglobin oxidation and lipid peroxidation in a very low concentration range (2.7-18 mg/mL). Furthermore, only stem bark extract (100 mg/mL) was able to inhibit the depletion of glutathione (13%). Discussion and conclusion: These results reinforce the therapeutic potential of stem bark and flower extracts of V. cauliflora to heal topical skin disease, namely in the treatment of neutrophil-related dermatosis and skin conditions related to oxidative stress, including skin aging.

show abstract

Oxidative DNA damage of peripheral blood polymorphonuclear leukocytes, selectively induced by chronic arsenic exposure, is associated with extent of arsenic-related skin lesions

Cited by 26 publications

References 35 publications

The mechanistic basis of arsenicosis: Pathogenesis of skin cancer

The mechanistic basis of arsenicosis: Pathogenesis of skin cancer

Arsenic-Induced Genotoxicity and Genetic Susceptibility to Arsenic-Related Pathologies

Stem bark and flower extracts ofVismia caulifloraare highly effective antioxidants to human blood cells by preventing oxidative burst in neutrophils and oxidative damage in erythrocytes

Contact Info

Product

Resources

About