Sepp Krisztián, Hausinger Péter, Hegedűs Béla, Kiss Péter Sándor, Cseszkó Edina, Mózes Miklós, Radács Marianna, Valkusz Zsuzsanna, Gálfi Márta, Molnár Zsolt
Department of Internal Medicine, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.
Department of Neurosurgery, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.
Biol Futur. 2025 May 2. doi: 10.1007/s42977-025-00256-4.
Calcipaenic bone disorders (e.g., osteoporosis) are becoming an epidemic as a significant public health concern. The underlying genetic, epigenetic, and homeostatic factors and the determinants of bone tissue expression are triggered by environmental exposures. Endocrine disruptor compounds are important in the development of pathological bone alterations. The aim of this study is to design an in vivo subtoxic chlorobenzene exposure model that can be used to explore certain bone changes and their consequences. Male Wistar rats were treated via gastric tube with a 1:1 mixture of hexachlorobenzene + 1,2,4-trichlorobenzene at a dose of 1.0 μg/kg bw; in a final volume of 1 mL, for 30, 60 and 90 days. Blood serum and bone samples were obtained from the femur diaphysis. The results of the treatments (n = 10/group) were interpreted as related to the controls. Serum levels of γGT, SGOT, SGPT were determined, along with bone tissue morphology, as well as the total mineral content of the bone and the mobilizable anorganic content. ANOVA was used to analyze the measurement data. As a result of the treatment protocol, histological examinations of bone morphology showed osteoid degeneration, as well as an altered state of the bone matrix. These findings are supported by the DEXA images, which showed a time-dependent decrease in surface mineral content, in parallel, an increase in the mobilizable anorganic content of the bone was detected. These results suggest that chlorobenzene administered may be a causal factor and changes in bone tissue structure can be traced.
钙缺乏性骨疾病（如骨质疏松症）正成为一种流行病，是一个重大的公共卫生问题。潜在的遗传、表观遗传和稳态因素以及骨组织表达的决定因素是由环境暴露引发的。内分泌干扰化合物在病理性骨改变的发展中很重要。本研究的目的是设计一种体内亚毒性氯苯暴露模型，可用于探索某些骨变化及其后果。雄性Wistar大鼠通过胃管给予六氯苯+1,2,4-三氯苯的1:1混合物，剂量为1.0μg/kg体重；终体积为1mL，持续30、60和90天。从股骨干骺端获取血清和骨样本。将治疗结果（每组n = 10）与对照组进行比较分析。测定血清γGT、SGOT、SGPT水平，以及骨组织形态、骨的总矿物质含量和可动员的无机含量。采用方差分析来分析测量数据。根据治疗方案，骨形态学的组织学检查显示类骨质变性以及骨基质状态改变。这些发现得到了双能X线吸收法（DEXA）图像的支持，该图像显示表面矿物质含量随时间下降，同时检测到骨的可动员无机含量增加。这些结果表明给予的氯苯可能是一个致病因素，并且可以追踪骨组织结构的变化。
