Direct exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increases infectivity of human erythrocytes to a malarial parasite.
Direct exposure to 10 nM 2,3,7,8-TCDD caused a 75% increase and a 2-fold increase in the infectivity of isolated human erythrocytes to P. falciparum after 48 hours when the parasites were in an unsynchronized or synchronized state of growth, respectively. Treatment of human erythrocytes with 10 microM sodium orthovanadate (NaOV), an inhibitor of plasma membrane Ca-ATPase and phosphotyrosine phosphatase, decreased parasitemia by 30%. Co-treatment of RBCs with TCDD and NaOV completely blocked the TCDD-induced increase in parasitemia. Because erythrocytes are anucleated, these results are discussed as evidence for biochemical changes by TCDD without requiring the activation of gene products.
Kim
H M
HM
Medical College of Virginia/V.C.U., Richmond.
Choi
I P
IP
Holsapple
M P
MP
D000818:Animals; D004912:Erythrocytes / Q000187:drug effects* / Q000469:parasitology; D006801:Humans; D010963:Plasmodium falciparum / Q000254:growth & development*; D000072317:Polychlorinated Dibenzodioxins / Q000633:toxicity*; D018336:Receptors, Aryl Hydrocarbon / Q000235:genetics / Q000502:physiology
D000072317:Polychlorinated Dibenzodioxins; D018336:Receptors, Aryl Hydrocarbon