In vitro and in vivo investigations on arsenic-induced cartilage degeneration in osteoarthritis

on the role of As in causing OA in mice. We employed chemical inhibition and inductively coupled plasma mass spectrometry analyses to identify the effect of As on chondrocytes as well as studying its accumulation in organs after oral administration in mice. Additionally, the study examined the effect of intra-articular As treatment on the levels of crucial catabolic factors, namely Hif-2 alpha (Epas1) and Zip8 (Slc39a8), during OA progression. Mice that were administered As orally in conjunction with surgically induced joint instability, had heightened cartilage destruction compared to wild-type mice. Quantitative analysis revealed a significant increase in Hif-2 alpha and Zip8 mRNA expression (p = 0.0352,0.0004 respectively) and protein expression (p = 0.0101,0.008 respectively) post oral administration. Our findings illustrated the role of As in influencing crucial cellular functions that are triggered by reactive oxygen species. These events consequently activate the Akt/Hif-2 alpha/NF-KB pathways, leading to disruptions in articular cartilage homeostasis. This study provides a comprehensive understanding of the impact of As on the development of osteoarthritis.

Automated summary

The study explores the role of arsenic (As) in the development of osteoarthritis (OA) in mice. Through chemical inhibition and inductively coupled plasma mass spectrometry analyses, the researchers identified the effects of As on chondrocytes and its accumulation in organs after oral administration. The findings show that As leads to heightened cartilage destruction and influences crucial cellular functions, activating specific pathways that disrupt articular cartilage homeostasis.