Response of the incisor tooth to 2,3,7,8-tetrachlorodibenzo-p-dioxin in a dioxin-resistant and a dioxin-sensitive rat strain

被引:29
作者
Kiukkonen, A
Viluksela, M
Sahlberg, C
Alaluusua, S
Tuomisto, JT
Tuomisto, J
Lukinmaa, PL
机构
[1] Univ Helsinki, Inst Dent, Dept Oral Pathol, FIN-00014 Helsinki, Finland
[2] Univ Helsinki, Inst Dent, Dept Pedodont & Orthodont, Helsinki, Finland
[3] Natl Publ Hlth Inst, Dept Environm Hlth, Kuopio, Finland
[4] Univ Helsinki, Cent Hosp, Dept Oral & Maxillofacial Dis, Helsinki, Finland
[5] Univ Helsinki, Cent Hosp, Dept Pathol, Helsinki, Finland
关键词
dioxins; 2; 3; 7; 8-tetrachlorodibenzo-p-dioxin; rat incisor; dentin; enamel; odontoblasts; enamel organ; dental defect; dose response; aryl hydrocarbon receptor;
D O I
10.1093/toxsci/69.2.482
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
Dioxins are ubiquitous environmental pollutants that afflict developing teeth. To find out if the effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the continuously erupting rat incisor is associated with the sensitivity to TCDD acute lethality and to see the histological basis for any macroscopic findings, we exposed 25 resistant Han/Wistar (Kuopio; H/W) and 20 sensitive Long-Evans (Turku/AB; L-E) female rats to total doses of 0.17, 1.7, 17, and 170 (only H/W rats) mug/kg TCDD. Each dose group comprised five animals. The treatment was started when the rats were 10 weeks old and continued for 20 weeks. The exposure time covered two life cycles of the incisor. Stereomicroscopic examination of the dissected mandibles showed color defects and pulpal perforation of the lower incisors at 17 and 170 mug/kg TCDD. Tissue sections revealed odontoblastic and pulpal cell death and the consequent arrest of dentin formation at the incisal tooth end at the same doses. H/W rat incisors were affected closer to the germinative tooth end at 170 than at 17 mug/kg TCDD, resulting in a larger perforation. In accordance with the enamel discoloration, the postsecretory enamel organ underwent, albeit inconsistently, precocious squamous metaplasia with pronounced proliferation. Thus, both the mesenchymal and, to a lesser extent, epithelial elements of the forming tooth were affected dose-dependently at relatively high doses of TCDD. Similar responses in both strains implied that the impaired formation of the incisor tooth, at least of its mesenchymal elements, is not associated with the differential resistance of H/W and L-E rats to TCDD acute lethality.
引用
收藏
页码:482 / 489
页数:8
相关论文
共 36 条
[1]   AH RECEPTOR IN EMBRYONIC MOUSE PALATE AND EFFECTS OF TCDD ON RECEPTOR EXPRESSION [J].
ABBOTT, BD ;
PERDEW, GH ;
BIRNBAUM, LS .
TOXICOLOGY AND APPLIED PHARMACOLOGY, 1994, 126 (01) :16-25
[2]   Developing teeth as biomarker of dioxin exposure [J].
Alaluusua, S ;
Lukinmaa, PL ;
Torppa, J ;
Tuomisto, J ;
Vartiainen, T .
LANCET, 1999, 353 (9148) :206-206
[3]   EXPOSURE TO 2,3,7,8-TETRACHLORODIBENZO-PARA-DIOXIN LEADS TO DEFECTIVE DENTIN FORMATION AND PULPAL PERFORATION IN RAT INCISOR TOOTH [J].
ALALUUSUA, S ;
LUKINMAA, PL ;
POHJANVIRTA, R ;
UNKILA, M ;
TUOMISTO, J .
TOXICOLOGY, 1993, 81 (01) :1-13
[4]   Polychlorinated dibenzo-p-dioxins and dibenzofurans via mother's milk may cause developmental defects in the child's teeth [J].
Alaluusua, S ;
Lukinmaa, PL ;
Vartiainen, T ;
Partanen, M ;
Torppa, J ;
Tuomisto, J .
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY, 1996, 1 (03) :193-197
[5]  
[Anonymous], DENT ANATOMY EMBRYOL
[6]   2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes an Ah receptor-dependent and ARNT-independent increase in membrane levels and activity of p60(Src) [J].
Blankenship, A ;
Matsumura, F .
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY, 1997, 3 (03) :211-220
[7]  
Bryant PL, 1997, TERATOLOGY, V55, P326
[8]   Correlation of 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced apoptotic cell death in the embryonic vasculature with embryotoxicity [J].
Cantrell, SM ;
Joy-Schlezinger, J ;
Stegeman, JJ ;
Tillitt, DE ;
Hannink, M .
TOXICOLOGY AND APPLIED PHARMACOLOGY, 1998, 148 (01) :24-34
[9]  
DAVIDEAU JL, 1995, INT J DEV BIOL, V39, P605
[10]  
Enan E, 1998, J BIOCHEM MOL TOXIC, V12, P263, DOI 10.1002/(SICI)1099-0461(1998)12:5<263::AID-JBT2>3.0.CO