Neuroprotection from Delayed Postischemic Administration of a Metalloporphyrin Catalytic Antioxidant

G. Burkhard Mackensen; Manisha Patel; Huaxin Sheng; Carla L. Calvi; Ines Batinić-Haberle; Brian J. Day; Li Ping Liang; Irwin Fridovich; James D. Crapo; Robert D. Pearlstein; David S. Warner

doi:10.1523/JNEUROSCI.21-13-04582.2001

Table 1.

A comparison of MnTE-2-PyP⁵⁺ activities to other antioxidants

Antioxidants	Redox potential (Mn^III/Mn^II) (E_1/2,V)^1-a	SOD (U SOD/mmol)^1-b	Catalase (sec⁻¹)^1-c	Lipid peroxidation inhibition (IC₅₀, μm)^1-d
Cu,Zn-SOD	+0.35^1-e	1.6 × 10⁸^f	—	15^g
MnTM-4-PyP⁵⁺	+0.06^f	5.4 × 10⁵^f	34	16^g
MnTE-2-PyP⁵⁺	+0.23^f	1.0 × 10⁷^f	128	1

^F1-aMetal-centered redox potentials versus normal hydrogen electrode obtained at pH 7.8 in 0.05m phosphate buffer, 0.1 m NaCI, 0.5 mm porphyrin, and related to Mn^III/Mn^II, redox couple.

^F1-bUnit of SOD activity (U SOD) is defined as the amount of antioxidant that inhibits one-half the reduction of cytochrome c by superoxide.

^F1-cActivity is presented as a first-order rate constant of hydrogen peroxide decay in the presence of varying concentrations of metalloporphyrins in 1 mmhydrogen peroxide at pH 7.8.

^F1-dThe concentration of antioxidant that inhibited 50% of iron–ascorbate initiated lipid peroxidation of a rat brain homogenate using thiobarbaturic acid reactive species as an index of lipid peroxidation.

^F1-e^,f,gData from these antioxidants have been published previously (Lawrence and Sawyer, 1979;Batinić-Haberle et al., 1999; Day et al., 1999, respectively).