Environmental exposure is a complex mixture of hazardous compounds with different mechanisms of toxicity. In case of concomitant exposure to carcinogenic substances--such as polycyclic aromatic hydrocarbons (PAHs)--and to heavy metals--such as lead (Pb)--the level of DNA damage may be enhanced. Children are considered more vulnerable than adults to chemical toxicants because they take in more toxicants as a proportion of body mass and because of inherent biological growth and developmental factors. The objective of the study was to measure cytogenetic effects in Silesian children and to investigate their relation with the environmental exposure to PAHs and Pb. The examined population included 74 children 5-14-year-old who lived in two cities located in the most polluted centre of the Silesia province. Individual exposure to lead was assessed for each child by measuring lead in blood (PbB), and to PAH by measuring 1-hydroxypyrene in urine (1-OHP), urinary mutagenicity and DNA adducts in circulating lymphocytes. Biomarkers of genetic effects were assessed by measuring micronuclei (MN) and sister chromatid exchanges (SCE) in children's peripheral lymphocytes. The mean levels of biomarkers of exposure were as follows: PbB 7.69 microg/dl, DNA adducts 9.59 adducts per 10(8) nt, 1-OHP 0.54 micromol/mol creatinine, and urinary mutagenicity presented as the number of revertants per mmol of creatinine: 485 for TA 98 and 1318 for YG1024. Mean value of MN was 4.44 per 1000 binucleated cells and SCE frequency ranged between 6.24 and 10.06 with a mean value of 7.87. The results suggest the influence of exposure to environmental agents on the induction of cytogenetic effects in peripheral lymphocytes of children: namely Pb on MN and PAHs on SCE. The sources of that exposure may be outdoor and indoor. Emissions from coal-burning stoves are important contributors to the total exposure to PAHs and Pb in Silesian children.
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http://dx.doi.org/10.1093/mutage/gel037 | DOI Listing |
Environ Epigenet
December 2024
Institute of Clinical Science B, Royal Victoria Hospital, Centre for Public Health, Queens' University Belfast, Grosvenor Rd, Belfast BT12 6BA, United Kingdom.
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November 2024
Indian Institute of Public Health-Bengaluru, Public Health Foundation of India, Bangalore, India.
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Metabol Open
March 2025
Department of Biochemistry and Microbiology, University of Zululand, KwaDlangezwa, 3886, South Africa.
Dyslipidemia is a prominent pathological feature responsible for oxidative stress-induced cardiac damage. Due to their high antioxidant content, dietary compounds, such as aspalathin and sulforaphane, are increasingly explored for their cardioprotective effects against lipid-induced toxicity. Cultured H9c2 cardiomyoblasts, an in vitro model routinely used to assess the pharmacological effect of drugs, were pretreated with the dietary compounds, aspalathin (1 μM) and sulforaphane (10 μM) before exposure to palmitic acid (0.
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March 2025
Central Department of Biotechnology, Tribhuvan University, Kirtipur, Nepal.
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January 2025
Department of Psychology and Neuroscience, Baylor University, Waco, TX, United States.
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