Lack of connexin 32 does not enhance the benzene-induced hematotoxicity and hemopoietic tumor incidence in mice

Yoon, Byung-IL

Korean Journal of Veterinary Research 2005;45(4):517-525.

Department of Veterinary Medicine and Institute of Veterinary Science, Kangwon National University

Abstract

This study was performed to evaluate using wild-type (WT) and $C{ imes}32$ knockout (KO) mice if lack of cell to cell communication by connexin 32 gap junction enhances the benzene-induced hematotoxicity and hemopoietic tumor development. The WT and $C{ imes}32$ KO mice were exposed to 300 ppm of benzene for 6 hours/day, 5 days/week for a total of 26 weeks by inhalation, and then sacrificed to evaluate the toxicities of hemopoietic organs or allowed to live out their life span to evaluate the hemopoietic tumor incidence. The significant increase and decrease of organ weight were respectively noted in spleen and thymus of both WT and $C{ imes}32$ KO mice without significant difference between the genotypes. Histopathologically, benzene exposure for 26 weeks induced the morphological changes in hemopoietic organs, characterized by fat cell accumulation in the bone marrow and extramedullary hemopoiesis in the spleen. The fat cell accumulation was, compared with that of WT mice, considerably exacerbated in the $C{ imes}32$ KO mice. However, no significant difference was observed in the changes of hematological values and bone marrow cellularity as well as in the onset and incidence of hemopoietic tumors between WT and $C{ imes}32$ KO mice. In conclusion, this study indicated little significant role of the cellular communication by $C{ imes}32$ gap junction in the action mechanism of benzene hematotoxicity and leukemogenicity.

Key Words: benzene, connexin 32, hematotoxicity, hemopoietic tumor