Free Radical Sponge

The applications of buckminsterfullerene C60 and derivatives in orthopaedic research

Qihai Liu 1, Quanjun Cui, Xudong Joshua Li, Li Jin

Abstract Buckminsterfullerene C60 and derivatives have been extensively explored in biomedical research due to their unique structure and unparalleled physicochemical properties. C60 is characterized as a “free radical sponge” with an anti-oxidant efficacy several hundred-fold higher than conventional anti-oxidants. Also, the C60 core has a strong electron-attracting ability and numerous functional compounds with widely different properties can be added to this fullerene cage. This review focused on the applications of C60 and derivatives in orthopaedic research, such as the treatment of cartilage degeneration, bone destruction, intervertebral disc degeneration (IVDD), vertebral bone marrow disorder, radiculopathy, etc., as well as their toxicity in vitro and in vivo.

Reduce Inflammation

Fullerol nanoparticles suppress inflammatory response and adipogenesis of vertebral bone marrow stromal cells–A potential novel treatment for intervertebral disc degeneration

Qihai Liu, PhD, Li Jin, MD, PhD, Francis H. Shen, MD, Gary Balian, PhD, and Xudong Joshua Li, MD, PhD

In conclusion, we believe that this is the first observation that fullerol, a potent antioxidant agent, suppresses IL-1 β-induced ROS and inflammatory cytokine production, inhibits the adipogenic differentiation of vBMSCs in vitro and, therefore, may prevent vertebral fatty marrow deposition and inflammatory responses during disc degeneration.

Improves cognition and extends the lifespan of mice

A carboxyfullerene SOD mimetic improves cognition and extends the lifespan of mice

Kevin L. Quick a, Sameh S. Ali a, Robert Arch b, Chengjie Xiong c, David Wozniak d, Laura L. Dugan a,

Abstract
In lower organisms, such as Caenorhabditis elegans and Drosophila, many genes identified as key regulators of aging are involved in
either detoxification of reactive oxygen species or the cellular response to oxidatively-damaged macromolecules. Transgenic mice have been
generated to study these genes in mammalian aging, but have not in general exhibited the expected lifespan extension or beneficial behavioral
effects, possibly reflecting compensatory changes during development. We administered a small-molecule synthetic enzyme superoxide
dismutase (SOD) mimetic to wild-type (i.e. non-transgenic, non-senescence accelerated) mice starting at middle age. Chronic treatment not only reduced age-associated oxidative stress and mitochondrial radical production, but significantly extended lifespan. Treated mice also exhibited improved performance on the Morris water maze learning and memory task. This is to our knowledge the first demonstration that an administered antioxidant with mitochondrial activity and nervous system penetration not only increases lifespan, but rescues age-related cognitive impairment in mammals. SOD mimetics with such characteristics may provide unique complements to genetic strategies to study the contribution of oxidative processes to nervous system aging.
© 2006 Elsevier Inc. All rights reserved.