Dietary amelioration of locomotor, neurotransmitter and mitochondrial aging

Exp. Biol. Med. 2010;235:66-76
doi:10.1258/ebm.2009.009219
© 2010 Society for Experimental Biology and Medicine

 

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Dietary amelioration of locomotor, neurotransmitter and mitochondrial aging

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Dietary amelioration of locomotor, neurotransmitter and mitochondrial aging
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Dietary amelioration of locomotor, neurotransmitter and mitochondrial aging

Articles by Aksenov, V.

Articles by Rollo, C D.
Dietary amelioration of locomotor, neurotransmitter and mitochondrial aging
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Dietary amelioration of locomotor, neurotransmitter and mitochondrial aging
Dietary amelioration of locomotor, neurotransmitter and mitochondrial aging

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Vadim Aksenov1,
Jiangang Long2,,
Sonali Lokuge1,
Jane A Foster3,
Jiankang Liu2 and
C David Rollo1,


1 Department of Biology, McMaster University 1280 Main St W, Hamilton, Ontario, Canada L8S 4K1
2 Institute of Mitochondrial Biology and Medicine, Department of Biology and Engineering, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Xi’an Jiaotong University School of Life Science and Technology, Xi’an 710049, China
3 Department of Psychiatry and Behavioural Neuroscience, McMaster University and Brain-Body Institute, St Joseph’s Healthcare 50 Charlton Ave. E T3308, Hamilton, Ontario, Canada L8N 4A6



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Figure 1 Relationship between age (months) and total movement (min/24 h) for supplemented (n = 9) and untreated (n = 9) normal mice (Nr) and supplemented (n = 11) and untreated (n = 11) transgenic growth hormone mice (Tg); P values indicate significance of illustrated regression lines Nr untreated: y = 432.631 – 7.553 (age), P < 0.006; Nr supplemented: y = 476.808 – 1.150 (age), P = 0.702. Intercepts significantly differ: P < 0.0001; slopes marginally differ: P = 0.08 Tg untreated: y = 230.892 – 1.298 (age), P = 0.7758; Tg supplemented: y = 385.093 – 13.171 (age), P < 0.006. Intercepts significantly differ: P < 0.0001; slopes significantly differ: P < 0.05. Analysis of covariance (covariate = age) detected significant differences between supplemented and untreated Nr (P < 0.014) and between supplemented and untreated Tg (P < 0.02)



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Figure 2 Examples of NPY mRNA expression in whole-brain cross-sections of untreated and supplemented normal female mice at 1.5 and 2 years of age. Note the diffuse pattern of foci throughout the striatum and cortex and increases in their number and intensity in supplemented mice



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Figure 3 (a) Relationship between age and mitochondrial complex III activity in brains of untreated (n = 10) and supplemented (n = 11) normal mice. Both regressions were significant, and slopes significantly differed, P < 0.0003 Untreated: r = –0.656, linear regression: P < 0.04; complex III activity = 24.735 – 0.014 (age) Supplemented: r = 0.891, linear regression: P < 0.0003; complex III activity = 15.443 + 0.015 (age) (b) Although similar in pattern to normal mice, linear regression models for mitochondrial complex III in supplemented and untreated transgenic (Tg) mice were not significant (P = 0.16 and P = 0.22, respectively). Slopes marginally differed, P = 0.057. Note the apparent depression of complex III activity by the supplement in Tg mice younger than 150 days. Overall, transgenic complex III activity was 20% lower than in normal mice



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Figure 4 Transgenic growth hormone mice (Tg) expressed a complex ‘U’-shaped pattern of protein carbonyls in homogenate with age. Dietary treatment was not resolved for Tg groups so data were pooled and analyzed as a first-order polynomial. A sharp rise in carbonyls was apparent in the oldest Tg mice. In normal mice homogenate protein carbonyls showed no significant age-related pattern and a very weak trend for increase with age (pooled for clarity of comparison to Tg mice). The first-order polynomial fit for transgenic mice was as follows: carbonyls = 4907.9 – 20.09 (age) + 0.038 (age2), n = 18, r = 0.689, P < 0.009, where carbonyls are relative density slot-blot units, and age is in days



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Figure 5 Relationship of mitochondrial carbonyls to complex III activity in supplemented and untreated transgenic growth hormone mice (Tg). Regression analyses of supplemented mice did not obtain significance but the parabolic fit for untreated Tg mice was highly significant: carbonyls = 4710.06 – 508.55 (complex III) + 27.15 (complex III2), n = 8, r = 0.9109, P < 0.012

Dietary amelioration of locomotor, neurotransmitter and mitochondrial aging
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