Differential vulnerability of substantia nigra and corpus striatum to oxidative insult induced by reduced dietary levels of essential fatty acids

Abstract

Oxidative stress (OS) has been implicated in the etiology of certain neurodegenerative disorders. Some of these disorders have been associated with unbalanced levels of essential fatty acids (EFA). The response of certain brain regions to OS, however, is not uniform and a selective vulnerability or resilience can occur. In our previous study on rat brains, we observed that a two-generation EFA dietary restriction reduced the number and size of dopaminergic neurons in the substantia nigra (SN) rostro-dorso-medial. To understand whether OS contributes to this effect, we assessed the status of lipid peroxidation (LP) and anti-oxidant markers in both SN and corpus striatum (CS) of rats submitted to this dietary treatment for one (F1) or two (F2) generations. Wistar rats were raised from conception on control or experimental diets containing adequate or reduced levels of linoleic and α-linolenic fatty acids, respectively. LP was measured using the thiobarbituric acid reaction method (TBARS) and the total superoxide dismutase (t-SOD) and catalase (CAT) enzymatic activities were assessed. The experimental diet significantly reduced the docosahexaenoic acid (DHA) levels of SN phospholipids in the F1 (~28%) and F2 (~50%) groups. In F1 adult animals of the experimental group there was no LP in both SN and CS. Consistently, there was a significant increase in the t-SOD activity (p < 0.01) in both regions. In EF2 young animals, degeneration in dopaminergic and non-dopaminergic neurons and a significant increase in LP (p < 0.01) and decrease in the CAT activity (p < 0.001) were detected in the SN, while no inter-group difference was found for these parameters in the CS. Conversely, a significant increase in t-SOD activity (p < 0.05) was detected in the CS of the experimental group compared to the control. The results show that unbalanced EFA dietary levels reduce the redox balance in the SN and reveal mechanisms of resilience in the CS under this stressful condition.

Mitochondrial and Oxidative Stress Aspects in Hippocampus of Rats Submitted to Dietary n-3 Polyunsaturated Fatty Acid Deficiency After Exposure to Early Stress

“…A recent study was able to demonstrate that a transgenerational n-3 PUFAs deficiency increased lipid peroxidation, SOD and catalase activity in striatum and substantia nigra in different ways, even in different generations and development stages [71]. Taken together, our results concerning the effects of n-3 PUFAs deficiency in hippocampus shows the importance of this dietary content to maintain an effective redox balance in this structure.…”

Serotonin modulation in neonatal age does not impair cardiovascular physiology in adult female rats: Hemodynamics and oxidative stress analysis

“…Briefly, 0.3 M H 2 O 2 was added to a mixture containing 0.3 mg/ml of homogenate and 50 mM phosphate buffer (pH 7.0). A decrease in the H 2 O 2 levels was noted, following which the absorbance was measured at 240 nm for 3 min; the CAT activity was expressed as U/mg protein [33,34].…”

Can fish oil supplementation and physical training improve oxidative metabolism in aged rat hearts?

“…The principle of the assay is based on the determination of the rate constant (k) of H 2 O 2 decomposition, which under our conditions of temperature and pH was defined as 4.6 × 10 7 . The rate constant of the enzyme was determined by measuring change in absorbance (at 240 nm) per minute over a 4-minute period and the CAT activity was expressed as U/mg protein [33,34].…”

“…Supernatants (0.1 mg) collected from homogenized hearts following centrifugation were incubated with 880 μl sodium carbonate (0.05%, pH 10.2, 0.1 mM EDTA) at 37°C before development of the reaction by the addition of 30 mM epinephrine (in 0.05% acetic acid) and determined by measuring the kinetic of the inhibition of adrenaline autooxidation at 480 nm expressed at U/mg protein [32,33].…”