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1.
FIGURE 6.

FIGURE 6. From: Diacetylbis(N(4)-methylthiosemicarbazonato) Copper(II) (CuII(atsm)) Protects against Peroxynitrite-induced Nitrosative Damage and Prolongs Survival in Amyotrophic Lateral Sclerosis Mouse Model.

CuII(atsm) therapy prevents cytoplasmic TDP-43 pathology in SOD1G93A mice. A, Western blot of cytoplasmic pTDP-43. Veh, vehicle. B, quantitation of full-length cytoplasmic pTDP-43 levels in 230-day-old mouse spinal cord normalized to β-actin. Truncated C-terminal pTDP-43 was also detected in spinal cords. CuII(atsm) treatment significantly reduced full-length pTDP-43 accumulation as well as cytosolic C-terminal pTDP-43. Graphs represent the percentage of change when compared with WT vehicle controls. n is shown at bottoms of bars (mean ± S.E.). **, p < 0.01.

Cynthia P. W. Soon, et al. J Biol Chem. 2011 December 23;286(51):44035-44044.
2.
FIGURE 5.

FIGURE 5. From: Diacetylbis(N(4)-methylthiosemicarbazonato) Copper(II) (CuII(atsm)) Protects against Peroxynitrite-induced Nitrosative Damage and Prolongs Survival in Amyotrophic Lateral Sclerosis Mouse Model.

Effect of CuII(atsm) treatment on reactive gliosis. A, GFAP expression shown by immunostaining of lumbar spinal cords from vehicle (Veh)- or CuII(atsm)-treated wild-type (WT) or SOD1G93A mice. B and C, Western blot quantitation of GFAP levels in 230-day-old mouse spinal cord. D, Iba1 expression revealed by immunostaining of spinal cords from mice. E and F, Western blot quantitation of Iba1 expression at 230 days in spinal cord. These results show reduction of astrogliosis and microgliosis with CuII(atsm) administration in mice. *, p < 0.05, **, p < 0.01, ***, p < 0.001. Error bars indicate mean ± S.E.

Cynthia P. W. Soon, et al. J Biol Chem. 2011 December 23;286(51):44035-44044.
3.
FIGURE 1.

FIGURE 1. From: Diacetylbis(N(4)-methylthiosemicarbazonato) Copper(II) (CuII(atsm)) Protects against Peroxynitrite-induced Nitrosative Damage and Prolongs Survival in Amyotrophic Lateral Sclerosis Mouse Model.

CuII(atsm) action on peroxynitrite. A, molecular structure of CuII(atsm). B, SOD activity was measured as the ability to inhibit pyrogallol oxidation determined by absorbance at 420 nm after a 1-h incubation. 10 units/ml SOD1 was able to inhibit ∼80% of pyrogallol oxidation. SOD1 activity was inhibited by the addition of 1 μm peroxynitrite (ONOO) and rescued by 1 μm CuII(atsm). Data shown are an average of three experiments and expressed as mean ± S.E. One-way analysis of variance with Dunnett's post hoc test was used for statistical analysis, **, p < 0.01, ***, p < 0.001 difference when compared with SOD1 + ONOO treatment.

Cynthia P. W. Soon, et al. J Biol Chem. 2011 December 23;286(51):44035-44044.
4.
FIGURE 2.

FIGURE 2. From: Diacetylbis(N(4)-methylthiosemicarbazonato) Copper(II) (CuII(atsm)) Protects against Peroxynitrite-induced Nitrosative Damage and Prolongs Survival in Amyotrophic Lateral Sclerosis Mouse Model.

Effect of CuII(atsm) on symptom onset, progression, and survival in SOD1G93A mice. A, Kaplan-Meier survival analysis of CuII(atsm)- and vehicle-treated SOD1G93A mice dosed at presymptomatic (Pre-sym) age. CuII(atsm) extended lifespan of SOD1G93A mice from 263 ± 3.4 days to 300 ± 10.8 days (mean ± S.E.), p < 0.001. B and C, motor function assessed by rotarod was significantly improved in drug-treated mice when compared with controls with delayed onset at 256 ± 3.9 days versus 237 ± 1.7, p < 0.001. D, onset of weight loss determined by age of decline from peak body weight. E, Kaplan-Meier survival curves for CuII(atsm) treatment started at symptomatic (Sym) age showing a 25-day extension, p < 0.001. In either study, there were no sex-related differences in survival time.

Cynthia P. W. Soon, et al. J Biol Chem. 2011 December 23;286(51):44035-44044.
5.
FIGURE 4.

FIGURE 4. From: Diacetylbis(N(4)-methylthiosemicarbazonato) Copper(II) (CuII(atsm)) Protects against Peroxynitrite-induced Nitrosative Damage and Prolongs Survival in Amyotrophic Lateral Sclerosis Mouse Model.

Effect of CuII(atsm) on motor neuron degeneration in SOD1G93A mice. A, micrographs of cresyl violet-stained lumbar spinal cord sections from wild-type (WT), vehicle (Veh)-, or CuII(atsm)-treated SOD1G93A mice. Higher magnification is shown in the insets. CuII(atsm)-treated mice exhibit larger, intact neuronal morphology when compared with vehicle-treated mice with atrophied and degenerating neurons. B, motor neuron numbers showing that CuII(atsm) treatment significantly attenuated neurodegeneration at 200 and 230 days when compared with vehicle group. Vehicle-treated SOD1G93A mice undergo significant motor neuron depletion at 200 and 230 days of disease when compared with wild-type mice. C and D, neurofilament expression determined by Western blot analysis of 230-day-old spinal cord showing restoration of neurofilament levels reflecting preservation of motor neurons with CuII(atsm) treatment, *, p < 0.05, **, p < 0.01, ***, p < 0.001. Error bars indicate mean ± S.E. The motor neuron counts were indistinguishable between vehicle- and CuII(atsm)-treated WT mice; therefore, these groups are pooled for the analysis.

Cynthia P. W. Soon, et al. J Biol Chem. 2011 December 23;286(51):44035-44044.
6.
FIGURE 3.

FIGURE 3. From: Diacetylbis(N(4)-methylthiosemicarbazonato) Copper(II) (CuII(atsm)) Protects against Peroxynitrite-induced Nitrosative Damage and Prolongs Survival in Amyotrophic Lateral Sclerosis Mouse Model.

Impact of CuII(atsm) treatment on oxidative and nitrosative stress indices in SOD1G93A mouse spinal cord. A, protein carbonyl levels were determined using OxyELISA in 230-day-old mice and normalized to protein levels. The data are expressed as the percentage of change over vehicle (Veh)-treated wild-type mice. B, 3-NT levels were determined by ELISA and normalized to protein levels. The data are expressed as the percentage of change over vehicle-treated wild-type mice. 3-NT levels were increased in SOD1G93A mice when compared with wild types and reduced with CuII(atsm) treatment. C, SOD1 enzymatic activity gel analysis of spinal cords. An equal amount of protein was loaded for WT (10 μg) and SOD1G93A (2 μg) mice, respectively. D, quantitation of SOD1 activity expressed relative to respective vehicle-treated groups. CuII(atsm) treatment significantly increased SOD1 activity when compared with vehicle-treated transgenic mice. WT, non-transgenic (Non TG) littermate of the SOD1G93A mice. n is shown at bottom of bars (mean ± S.E.). One-way analysis of variance with Tukey's post hoc test, *, p < 0.05, **, p < 0.01, ***, p < 0.001 difference. ns, not significant.

Cynthia P. W. Soon, et al. J Biol Chem. 2011 December 23;286(51):44035-44044.

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