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The central nervous system (CNS) utilizes oxygen more intensely than other organs and is characterized by a relatively low activity of antioxidant defense (AOD) enzymes [1,2].Human aging is accompanied by a decrease in AOD along with an increase in the monoamine oxidase B (MAO-B) activity in the brain [3][4][5]. The age-related increase in MAO-B activity is thought to aggravate the initial deficiency of cerebral AOD [3][4][5]. Another picture is observed in the spinal cord, where AOD decreases dramatically notwithstanding the absence of age-related changes in . Regardless of the causes of AOD suppression with age, AOD insufficiency decreases the resistance to oxidative stress (OS) and allows induction of lipid peroxidation (LPO), one of the key mechanisms of ischemic death and apoptosis of neurons [2]. The known heterochronism of involution in different parts of the CNS [5] can be related with local features of OS sensitivity and contents of LPO products.In the present work, age-related changes in these parameters were studied in different parts of the human brain and spinal cord. METHODSPreparations of the CNS were obtained as autopsy material from 63 men and 15 women who died suddenly at the age of 22-92 years. The material was obtained from the Chelyabinsk Regional Bureau of Forensic Medical Examination. Cases of a lethal outcome of coronary or cerebral thrombosis were excluded. Samples of nervous tissue with signs of ischemic or hemorrhagic insult were excluded. The deaths were most often caused by accidents (road accidents, falls from a height, etc.). The material to be studied was taken no later than 12 h after the death. This time was chosen on the basis of data on stable activities of the AOD enzymes during this period [5]. Four age groups were set: first adult (women of 21-35 and men of 22-35 years), second adult (women of 36-55 and men of 36-60 years), elderly (women of 56-74 and men of 61-74 years), and senile (75 or more years of age).LPO was studied in several structures of the brain and spinal cord. In the brain, we examined two regions of the hemispheric cortex (fields 6 and 17), basal ganglia (the pale globe, caudate nucleus, and putamen), diencephalic structures (the thalamus and hypothalamus), the cerebellum, the mesencephalon, and the myelencephalon. In the spinal cord, we studied the cervical enlargement, the thoracal part, and the sacrolumbar enlargement.Contents of LPO products were determined using extraction and spectrophotometry, separately in the heptane and isopropanol phases of the lipid extract [7]. This approach allowed us to differentially determine acyl peroxides in phospholipids extracted with isopropanol and nonesterified intermediates of fatty acid peroxidation in the heptane phase. The results were expressed in oxidation index units as Ö 232 /Ö 220 (the relative content of diene conjugates (DC)) and Ö 278 /Ö 220 (the levels of ketodienes (KD) and triene conjugates (TC), respectively). The content of LPO final products, Schiff bases (SB), was determined in both phases of the lip...

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Activities of monoamine oxidase B, Cu-Zn-dependent superoxide dismutase (SOD), and catalase, the concentration of enzyme-active ceruloplasmin, and resistance of the nerve tissue to oxidative stress were examined in spinal cord preparations from humans (n=43) died at the age of 21-92 years. Age-related activation of monoamine oxidase B was found only in thoracic segments, while age-related decrease in SOD activity was demonstrated in thoracic segments and cervical intumescence of the spinal cord. Age-related accumulation of enzyme-active ceruloplasmin was observed in all segments of the spinal cord. Activation of catalase and increased sensitivity to oxidative stress were observed in the cervical and lumbosacral intumescences. Heterotopic changes in the examined indices suggest that activity of monoamine oxidase B cannot serve as a universal factor of age-related changes in antioxidant defense in the spinal cord and its sensitivity to oxidative stress.

A direct correlation was found between the content of oxidative protein modification products in the cervical enlargement of the spinal cord and age in humans. We revealed a considerable increase in Cd(2+) concentrations in elderly and old people and an increase in Fe(2+) concentration in old people. In the lumbosacral enlargement Cd(2+) concentration was maximum and did not vary with age. The content of oxidative protein modification products significantly increased in the lumbosacral enlargement in older adults and old people. Moreover, old people had high content of Cu(2+) in the lumbosacral enlargement. Our findings suggest that accumulation of Cd(2+) play a role in the metabolism of Cu(2+) and Fe(2+), which contributes to age-related intensification of oxidative protein modification in the spinal cord.