Abstrak
Effect Of Lead Nanoparticles Inhalation On Mesostructure And The Osteoprotegerin/Receptor Activator Of Nuclear Factor-Kappab Ligand System In Rats
Rendra Leonas, Zairin Noor, Hermawan Nagar Rasyid, Tita Husnitawati Madjid, Fachry Ambia Tanjung
Universitas Padjadjaran, Cukurova Med J 2017;42(1):48-54, DOI: 10.17826/cutf.280083
Bahasa Inggris
Universitas Padjadjaran, Cukurova Med J 2017;42(1):48-54, DOI: 10.17826/cutf.280083
bone remodeling, femur., inhalation, toxicology
Purpose: This study aims to investigate whether Pb nanoparticle exposure affects the mesostructure, and osteoprotegerin/receptor activator of nuclear factorkappaB ligand (OPG/RANKL) system in rats exposed to subchronic and chronic inhalation. Material and Methods: Forty eight rats were randomly divided into eight groups. One group is a non-exposed group. While three groups were exposed to nanoparticles Pb at the following doses 6.25; 12.5; or 25 mg/m3 an hour daily for 28 days. Another three groups were exposed to nanoparticles Pb at following doses 6.25; 12.5; and 25 mg/m3 one hour daily for 6 months. Results: Subchronic and chronic Pb nanoparticles changed trabecular mesostructure. We found that subchronic exposure significantly increased the levels of OPG at the first and second dose exposure compared to the control groups (P < 0.05). In the chronic exposure, we found that the levels of OPG significantly increased at the first and second dose exposure compared to the control group (P < 0.05). In this study significant reduction in subchronic exposure to second and third doses compared to the first dose or exposure control (P < 0.05) were shown. In chronic exposure, no significant differences in RANKL levels were found between groups (P > 0.05). In subchronic exposure, the ratio of OPG/RANKL significantly increased between the third dose exposure compared to controls (P < 0.05), with not significant differences in chronic exposure. Conclusion: Pb nanoparticle induced trabecular bone neoformation at least a part via OPG stimulation and inhibition of RANKL by osteoblast.