RESUMO
Exposure to pesticides has been linked to an elevated risk of leukemia. The present research aimed to evaluate the relationship between organochlorine (OC) pesticides and biomarkers of oxidative stress in leukemia patients. This work was conducted on 109 patients with leukemia and 109 healthy controls. The serum concentrations of seven derivatives of OCs including alpha-HCH, beta-HCH, gamma-HCH, 2,4-DDT, 4,4-DDT, 2,4-DDE, and 4,4-DDE along with acetylcholinesterase (AChE), glutathione peroxidase (GPx), superoxide dismutase (SOD), paraoxonase-1 (PON1), and catalase (CAT) activities as well as total antioxidant capacity (TAC), nitric oxide (NO), protein carbonyl (PC), and malondialdehyde (MDA) levels were measured in all the subjects. Levels of OCs were remarkably higher in leukemia patients compared to the controls (p < 0.05). In addition, levels of SOD, AChE, GPx, PON-1, and TAC were remarkably lower in leukemia patients compared to controls (p < 0.05). In contrast, MDA, NO, and PC concentrations were higher in leukemia patients than in the controls (p < 0.05). Moreover, the serum level of 4,4-DDE was negatively associated with GPx activity (p = 0.038). Our findings suggest that OCs may play a role in the development of leukemia by disrupting the oxidant/antioxidant balance.
Assuntos
Hidrocarbonetos Clorados , Praguicidas , Antioxidantes/metabolismo , Acetilcolinesterase/metabolismo , Estudos de Casos e Controles , DDT , Estresse Oxidativo , Glutationa Peroxidase/metabolismo , Superóxido Dismutase , Biomarcadores , MalondialdeídoRESUMO
Exposure to organochlorines is associated with epigenetic changes, including methylation change in the promoter of tumor suppressor genes, thereby leading to cancer induction. The aim of this study was to investigate the relationship between organochlorine pesticides (OCPs) and ABL1 promoter methylation in child patients with acute lymphoblastic leukemia (ALL) and the control group. The methylation rate of the ABL1 promoter was evaluated using the methylation-specific polymerase chain reaction method, and the level of OCPs in patients with ALL and healthy children was measured using gas chromatography. ABL1 promoter hypermethylation was observed in 64% of ALL patients and 28.5% of children in the control group. The level of OCPs in children with methylated ABL1 promoters was significantly higher than that in children with nonmethylated ABL1 promoters (p < 0.05). Our findings suggest that OCPs, especially alpha-hexachlorocyclohexane, beta-hexachlorocyclohexane, gamma-hexachlorocyclohexane, 2,4 dichlorodiphenyldichloroethylene, and 4,4 dichlorodiphenyltrichloroethane may induce methylation at the ABL1 promoter level, thereby preventing the normal expression of the ABL1 gene. As a result, the reduced expression of ABL1 (a tumor suppressor) gene due to the hypermethylation of its promoter leads to the disruption of normal biological processes, thus making cells vulnerable to oncogenic factors.
Assuntos
Hidrocarbonetos Clorados , Praguicidas , Leucemia-Linfoma Linfoblástico de Células Precursoras , Proteínas Proto-Oncogênicas c-abl/metabolismo , Criança , Metilação de DNA/genética , Humanos , Hidrocarbonetos Clorados/toxicidade , Praguicidas/toxicidade , Leucemia-Linfoma Linfoblástico de Células Precursoras/genética , Regiões Promotoras Genéticas/genéticaRESUMO
Exposure to pesticides has been linked to an elevated risk of leukemia. The present research aimed to evaluate the relationship between organochlorine (OC) pesticides and biomarkers of oxidative stress in patients with leukemia. This work was conducted on 109 patients with leukemia and 109 healthy controls. The serum concentrations of seven derivatives of OCs including alpha-hexachlorocyclohexane (HCH), beta-HCH, gamma-HCH, 2,4-dichlorodiphenyltrichloroethane (DDT), 4,4-DDT, 2,4-dichlorodiphenyldichloroethylene (DDE), and 4,4-DDE along with acetylcholinesterase (AChE), glutathione peroxidase (GPx), superoxide dismutase (SOD), paraoxonase-1 (PON1), and catalase (CAT) activities as well as total antioxidant capacity (TAC), nitric oxide (NO), protein carbonyl (PC), and malondialdehyde (MDA) levels were measured in all the subjects. Levels of OCs were remarkably higher in patients with leukemia compared with the controls (p<0.05). In addition, levels of SOD, AChE, GPx, PON1, and TAC were remarkably lower in patients with leukemia compared with controls (p<0.05). In contrast, MDA, NO, and PC concentrations were higher in patients with leukemia than in the controls (p<0.05). Moreover, the serum level of 4,4-DDE was negatively associated with GPx activity (p=0.038). Our findings suggest that OCs may play a role in the development of leukemia by disrupting the oxidant/antioxidant balance.