p,p′-DDE, a DDT metabolite, induces proinflammatory molecules in human peripheral blood mononuclear cells “in vitro”

Cárdenas-González, Mariana; Gaspar-Ramírez, Octavio; Pérez‐Vázquez, Francisco Javier; Alegría-Torres, Jorge Alejandro; González‐Amaro, Roberto; Pérez-Maldonado, Iván N.

doi:10.1016/j.etp.2012.07.006

Cited by 25 publications

(15 citation statements)

References 41 publications

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“…Different authors have proved DDT to be hazardous to humans by using different tests [50][51][52][53][54][55]. Shaw et al [56] presented data on pesticide residues in milk from Indonesian women which demonstrated general exposure to p,p'-DDT and hexachlorobenzene (HCB).…”

Section: Toxicity Among Humansmentioning

confidence: 99%

Toxic Effects of Organochlorine Pesticides: A Review

Singh¹

2016

AJBIO

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This study is aimed at compiling the toxicological aspects of organochlorine compounds (OCCs) including pesticides among different animal models. Tests on animal species like Mean Probable Effect Concentration Quotient (PEC-Q) test, DNA repair assays and histopathological examinations have shown positive results for the toxicity of organochlorine pesticides. The results were observed on different animals including fishes, furseals, frogs, rats, bats and humans. In fishes, endosulfan is found to have acute toxicities. Similarly, organophosphorus, synthetic pyrethroids and microbial insecticides were also found to show their toxic effects. Some compounds such as lambda-cyhalothrin showed a very high toxicity on fish followed by fenvalerate, deltamethrin and cypermethrin. Exposure to OCCs can impart foe cell death by inducing Mitogen Activated Protein Kinase Pathway (MAPK) which is associated with cell growth differentiation and apoptosis. On studying the genotoxic effects of OCCs on germ cells of mouse, it was observed that a lethal mutation can occur just after one mating interval. Increase in the number of micronucleated cells has also been seen after OCC exposure. Neuro-behavioural studies on rats showed the presence of tremors caused by chlordecone and p,p'DDT. Tumorigenicity by organochlorine pesticides is seen to be an epigenetic mechanism in a DNA repair assay. Acute poisoning was seen in liver, kidney and testis of albino rat due to the toxic effect of dursban and DDT. Great declines in populations have been seen due to OCC toxicity in different animal species. Direct and indirect exposure to these compounds should be reduced so as to minimize the possible health hazards.

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Section: Toxicity Among Humansmentioning

confidence: 99%

Toxic Effects of Organochlorine Pesticides: A Review

Singh¹

2016

AJBIO

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“…In previous studies, it was demonstrated that 10 mg DDE/ml was able to induce pro-inflammatory cytokines in PBMC (Alegría-Torres et al, 2009;Cárdenas-González et al, 2013). Using this concentration to ascertain the effect of DDE on AhR mRNA expression (Figure 2A), it was seen that DDE induced a significant increase in AhR mRNA expression after 2 h of exposure compared to that seen in the NE cells.…”

Section: Resultsmentioning

confidence: 99%

DDE and PCB 153 independently induce aryl hydrocarbon receptor (AhR) expression in peripheral blood mononuclear cells

Gaspar-Ramírez

Pérez‐Vázquez

Salgado‐Bustamante³

et al. 2014

Journal of Immunotoxicology

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Recent studies have demonstrated that compounds inducing pro-inflammatory cytokines enhance AhR expression. The aim of this study was 2-fold: (1) to determine if two pro-inflammatory compounds, dichlorodiphenyldichloroethylene (DDE) and 2,2 0 ,4,4 0 ,5,5 0 -hexa-chlorobiphenyl (PCB 153), independently affect AhR gene expression in peripheral blood mononuclear cells (PBMC); and (2) if affected, to determine whether the mechanism involved was due to AhR activation or to a pro-inflammatory effect of the chemicals. PBMC isolated from healthy individuals were incubated in the presence of DDE (10 mg/ml) and PCB 153 (20 ng/ml) over time and AhR and CYP1A1 expression was assessed with a real-time PCR technique. The results indicated there was over-expression of the AhR mRNA in PBMC when the cells were treated with DDE and PCB 153. No changes in expression levels of CYP1A1 mRNA were found. Importantly, when the cells were exposed to DDE and PCB 153 in the presence of an antagonist of tumor necrosis factor (TNF)-, the over-expression of AhR was abolished; as expected, the expression of CYP1A1 was unaffected. In conclusion, these studies demonstrated for the first time an increment of AhR expression ''in vitro'' in PBMC treated with two pro-inflammatory environmental pollutants, DDE and PCB153. Moreover, the over-expression of AhR was dependent of TNF induced by DDE and PCB 153 and was independent of AhR activation.

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“…The literature has reported that DDE residue was detected in agricultural workers from Bolivia. The concentration of DDE in the serum and in their lipids was 19.7 ng/ml and 4788.7 ng/(g lipid), respectively, and it was shown to induce proinflammatory molecules in the human peripheral blood mononuclear cells due to its toxicity [6]. Furthermore, DDE was shown to cause serious environmental problems [7].…”

Section: Introductionmentioning

confidence: 99%