Therapeutic potential of nanocarbon c60 fullerene in osteoarthritis
International Journal of Development Research
Therapeutic potential of nanocarbon c60 fullerene in osteoarthritis
Received 15th January, 2017; Received in revised form 24th February, 2017; Accepted 22nd March, 2017; Published online 30th April, 2017
Copyright©2017, Kazuo Yudoh et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
In osteoarthritis (OA), mechanical stress on articular cartilage stimulates to produce excess amounts of reactive oxygen species (ROS). Studies have provided ample confirmation of the generation of ROS and the depletion of cellular antioxidants in degenerated articular cartilage. 8-Oxoguanine, an oxidized form of guanine, is produced by ROS in DNA. 8-oxoguanine is thought to be a major causative lesion for mutagenesis by ROS, since it can form a stable base pair with adenine as well as with cytosine during DNA replication. 8-Oxoguanine causes A:T to C:G and G:C to T:A transversion mutations. 8-Oxoguanine DNA glycosylase (Ogg1) repairs 8-oxoguanine. In the mitochondria, Ogg1 can protect against activation of the intrinsic apoptotic pathway in response to oxidative stress by augmenting DNA repair in a variety of cells. However, it still remains unclear whether the accumulation of 8-oxoguanine in the cells participates in the pathogenesis of oxidative stress-induced diseases such as OA. Recent reports demonstrated that an increase in 8-oxoguanine and a decrease in Ogg1 were observed in degenerated neural cells compared with normal neural cells in neurodegenerative diseases. We also observed that OA-related catabolic factor induced over expression of 8-oxoguanine and down regulation of Ogg1 in chondrocytes. In the previous studies, we have focused on nanocarbon molecule, fullerene (C60), which acts a strong free radical scavenger, as an anti-oxidant, to prevent the degeneration of articular cartilage. We have demonstrated that C60 has a potential as a protective agent against the degeneration of articular cartilage both in vitro and in vivo OA models. We also found that C60 increased the expressions of DNA repair enzyme Ogg1 in OA chondrocytes. From the results of previous reports, C60 may have a therapeutic potential, as a nanomedicine, to protect against the oxidative stress-induced diseases, through the mechanism involving the acceleration of expression of DNA repair enzyme Ogg1.
