Characterization of the Age Changes in Brain and Liver Enzymes of Senescence-Accelerated Mice (SAM)

Summary: Some enzymes and neurotransmitters have different activity in mice models of accelerated aging.

Interestingness: 1

Paper by E Bulygina, S Gallant, G Kramarenko, S Stvolinsky, M Yuneva and A Boldyrev in the Journal of Anti-Aging Medicine, Volume 2, Issue 1, Spring 1999.

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In senescence accelerated mice, prone 1 (SAMP1) compared to senescence accelerated mice, resistant 1 (SAMR1):

• Mono-amine oxide b (MAOb) activity in the brain goes up as it ages. In SAMR1 it stays put.
• Glutamate binding in N-methyl-D-aspartic acid (NMDA) receptors starts much lower in young mice, but climbs to be much higher as it ages
• Na/K ATPase activity in the brain goes up as it ages.
• Cytochrome P450 activity in the liver is consitently higher

In all of the above, young is 4 months, age tracking goes from 8-12 months. SAMP1 mice die around then.
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Abstract follows:

The comparative neurochemical characteristics of brain and liver membranes of senescence-accelerated mice, prone (SAMP1) and senescence-accelerated mice, resistant (SAMR1) strains were evaluated using males and females of several ages. Abnormal N-methyl-D-aspartic acid (NMDA) binding and monoamine oxidase b activity in SAMP brain membranes may promote increased accumulation of reactive oxygen species (ROS) in neurons. Na/K-adinosine triphosphatase (ATPase) and liver cytochrome P450 activities are greater in SAMP1 neurons than in SAMR1 neurons, which may reflect an adaptive tissue response to ROS accumulation.