A biologically effective fullerene (C60) derivative with superoxide dismutase mimetic properties

Ali, Sameh S.; Hardt, Joshua I.; Quick, Kevin L.; Kim-Han, Jeong Sook; Erlanger, Bernard F.; Huang, Ting‐Ting; Epstein, Charles J.; Dugan, Laura L.

doi:10.1016/j.freeradbiomed.2004.07.002

Cited by 345 publications

(247 citation statements)

References 45 publications

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“…H. 05) and increased susceptibility to toxin induced seizures (Liang and Patel, 2004). Increased cellular injury in these mouse models is prevented by SOD mimetics, confirming the direct role of SOD2 in enhancing disease phenotypes (Patel, 2003;Ali et al, 2004). Such evidence has led to heightened interest in the clinical application of antioxidants for neurological disorders, including DN (Paolisso et al, 1994;Natarajan et al, 2002;Henriksen, 2006;Coverley and Baxter, 1997).…”

Section: Discussionmentioning

confidence: 89%

SOD2 protects neurons from injury in cell culture and animal models of diabetic neuropathy

Vincent

Russell

Sullivan

et al. 2007

Experimental Neurology

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Hyperglycemia-induced oxidative stress is an inciting event in the development of diabetic complications including diabetic neuropathy. Our observations of significant oxidative stress and morphological abnormalities in mitochondria led us to examine manganese superoxide dismutase (SOD2), the enzyme responsible for mitochondrial detoxification of oxygen radicals. We demonstrate that over expression of SOD2 decreases superoxide (O 2 •− ) in cultured primary dorsal root ganglion (DRG) neurons and subsequently blocks caspase-3 activation and cellular injury. Under expression of SOD2 in dissociated DRG cultures from adult SOD2 +/− mice results in increased levels of O 2 •− , activation of caspase-3 cleavage and decreased neurite outgrowth under basal conditions that are exacerbated by hyperglycemia. These profound changes in sensory neurons led us to explore the effects of decreased SOD2 on the development of diabetic neuropathy (DN) in mice. DN was assessed in SOD2 +/− C57BL/6J mice and their SOD2 +/+ litter mates following streptozotocin (STZ) treatment. These animals, while hyperglycemic, do not display any signs of DN. DN was observed in the C57BL/6Jdb/db mouse, and decreased expression of SOD2 in these animals increased DN. Our data suggest that SOD2 activity is an important cellular modifier of neuronal oxidative defense against hyperglycemic injury.

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Section: Discussionmentioning

confidence: 89%

SOD2 protects neurons from injury in cell culture and animal models of diabetic neuropathy

Vincent

Russell

Sullivan

et al. 2007

Experimental Neurology

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“…The protective effects of fullerenes in vivo. The SODlike activity was responsible for significantly increasing the in utero survival of clonogenic DBA2J MnSOD -=À mice when dams were given 100 mg=kg=day of C 3 in a drinking water (of which 10% was absorbed); a 300% increase in postnatal survival was reported when C 3 was given SC to pups at 10 mg=kg (8). Data indicate that C 3 localizes in mitochondria, where it replaces MnSOD.…”

Section: Nonmetal-based Sod Mimicsmentioning

confidence: 95%

“…The use of fullerenes for biologic applications progressed as soon as the water-soluble derivatives emerged (162,280). Early studies suggested that direct reactions between hydroxyl, alkoxyl, alkylperoxyl, and benzyl radicals and the highly conjugated double-bond system of C 60 fullerenes were responsible for their antioxidant actions; however, the mechanism is not quite understood (8). SOD-like catalytic action was reported for a water-soluble derivative (C 3 ) that bears three malonyl residues on its surface (8).…”

Section: Nonmetal-based Sod Mimicsmentioning

confidence: 99%

“…Early studies suggested that direct reactions between hydroxyl, alkoxyl, alkylperoxyl, and benzyl radicals and the highly conjugated double-bond system of C 60 fullerenes were responsible for their antioxidant actions; however, the mechanism is not quite understood (8). SOD-like catalytic action was reported for a water-soluble derivative (C 3 ) that bears three malonyl residues on its surface (8). The k cat of 2Â10 6 M=s at pH 7.4 increases 10-fold per each pH unit decrease, as a protonation of the carboxylate moieties becomes favorable.…”

Section: Nonmetal-based Sod Mimicsmentioning

confidence: 99%

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Superoxide Dismutase Mimics: Chemistry, Pharmacology, and Therapeutic Potential

Batinić‐Haberle

Rebouças

Spasojević

2010

Antioxidants & Redox Signaling

456

677

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Oxidative stress has become widely viewed as an underlying condition in a number of diseases, such as ischemia-reperfusion disorders, central nervous system disorders, cardiovascular conditions, cancer, and diabetes. Thus, natural and synthetic antioxidants have been actively sought. Superoxide dismutase is a first line of defense against oxidative stress under physiological and pathological conditions. Therefore, the development of therapeutics aimed at mimicking superoxide dismutase was a natural maneuver. Metalloporphyrins, as well as Mn cyclic polyamines, Mn salen derivatives and nitroxides were all originally developed as SOD mimics. The same thermodynamic and electrostatic properties that make them potent SOD mimics may allow them to reduce other reactive species such as peroxynitrite, peroxynitrite-derived CO 3 _ À , peroxyl radical, and less efficiently H 2 O 2 . By doing so SOD mimics can decrease both primary and secondary oxidative events, the latter arising from the inhibition of cellular transcriptional activity. To better judge the therapeutic potential and the advantage of one over the other type of compound, comparative studies of different classes of drugs in the same cellular and=or animal models are needed. We here provide a comprehensive overview of the chemical properties and some in vivo effects observed with various classes of compounds with a special emphasis on porphyrin-based compounds. Antioxid. Redox Signal. 13, 877-918.

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“…The double bonds in the carbon can also be beneficial in the body with evidence that they can be used to remove superoxide radicals (O 2 À ) that cause tissue damage including strokes and cancer [33]. These are naturally generated in the body when neutrophils and immune cells attack pathogens in the body.…”

Section: Dlc In the Bodymentioning

confidence: 99%

Diamond like carbon coatings for potential application in biological implants—a review

Love

Cook

Harvey

et al. 2013

Tribology International

223

116

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a b s t r a c tProduction of wear debris has been linked to the failure of numerous hip implants. With the current focus on increasing the implant longevity, thus wear and corrosion resistance is important. Hard coatings have the potential to reduce the wear and corrosion. Diamond like Carbon (DLC) coatings exhibit properties that could make them viable for implants. This paper critically reviews previously published research into usage of DLC coatings for implants. Overall DLCs seem to be an effective coating for implants but with the variance in results, further testing is required for clarification of use.

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A biologically effective fullerene (C60) derivative with superoxide dismutase mimetic properties

Cited by 345 publications

References 45 publications

SOD2 protects neurons from injury in cell culture and animal models of diabetic neuropathy

SOD2 protects neurons from injury in cell culture and animal models of diabetic neuropathy

Superoxide Dismutase Mimics: Chemistry, Pharmacology, and Therapeutic Potential

Diamond like carbon coatings for potential application in biological implants—a review

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