RANKL: A Key Factor In Trichloroethylene Induced Toxicity In Rats

Trichlorethylene (TCE), a chlorinated solvent, is mainly used as an idealdegreaser and desiccant in the industrial production due to its good lipophilicity andlow melting point and TCE is also extensively used in family products such asadhesives, lubricants and correction fluid. Yet, without appropriate treating of TCEafter using it making a growing number of TCE becomes environmentalcontaminants, which endanger human’s health. TCE has a variety of roles, includingneurotoxicity, kidney damage, liver damage, lung damage, changes in heart rate,immune organ pathological changes. However, the mechanism of TCE toxicity isstill unknown. Therefore, TCE has been included in the China’s environmentalcharacteristics "blacklist" and involved in the U.S. Environmental ProtectionAgency129priority pollutants, which was published in1976.Receptor activator of nuclear factor-κB ligand (RANKL) is a member of thetumor necrosis factor family and its receptor is the receptor activator of nuclearfactor-κB (RANK). RANKL has multiple roles, including, bone remodeling, theprocess of the formation of the lymph nodes, the establishment of the thymicmicroenvironment, mammary gland development during pregnancy, hormones causebreast cancer， and cancer in bone metastasis.In this article we used oral administration of TCE to cause damages to the heart,liver, lung, kidney, spleen and thymus. Thereafter we utilized hematoxylin-eosinstaining, immunohistochemistry and Western-Blot methods to detect TCE toxicitydamages and RANKL expressions in the rats, in order to discover the correlationbetween the TCE toxic injuries and RANKL expressions. In this study we found thatTCE can significantly reduce the rats’ weight and food consumption, and exacerbateorgans’ histopathology morphologic damages and improve RANKL expressions indifferent tissues, suggesting that RANKL may be involved in the TCE toxic damagesto the body. This study provided a theoretical basis to the toxic effects of environmental toxins TCE and the mechanism of TCE toxicity.