Foods with Potential Prooxidant and Antioxidant Effects Involved in Parkinson's Disease

Abstract

Oxidative stress plays a fundamental role in the pathogenesis of Parkinson's disease (PD). Oxidative stress appears to be responsible for the gradual dysfunction that manifests via numerous cellular pathways throughout PD progression. This review will describe the prooxidant effect of excessive consumption of processed food. Processed meat can affect health due to its high sodium content, advanced lipid oxidation end-products, cholesterol, and free fatty acids. During cooking, lipids can react with proteins to form advanced end-products of lipid oxidation. Excessive consumption of different types of carbohydrates is a risk factor for PD. The antioxidant effects of some foods in the regular diet provide an inconclusive interpretation of the environment's mechanisms with the modulation of oxidation stress-induced PD. Some antioxidant molecules are known whose primary mechanism is the neuroprotective effect. The melatonin mechanism consists of neutralizing reactive oxygen species (ROS) and inducing antioxidant enzyme's expression and activity. N-acetylcysteine protects against the development of PD by restoring levels of brain glutathione. The balanced administration of vitamin B3, ascorbic acid, vitamin D and the intake of caffeine every day seem beneficial for brain health in PD. Excessive chocolate intake could have adverse effects in PD patients. The findings reported to date do not provide clear benefits for a possible efficient therapeutic intervention by consuming the nutrients that are consumed regularly.

Figure 1

Schematic representation of the oxidative stress mechanism in the development of Parkinson's disease in dopaminergic neurons. Oxidative stress from aging or exogenous sources causes damage to vulnerable cellular structures such as mitochondria and DNA. α-Synuclein gene mutations can promote the formation of α-synuclein oligomers and Lewis bodies. Oxidative stress causes mitochondrial dysfunction that converts the mitochondria into a source of ROS/RNS. ROS/RNS increases α-synuclein aggregate formation, and these, in turn, damage mitochondrial function. Both mitochondrial dysfunction and Lewis bodies lead to a loss of dopaminergic neurons and thus neurodegeneration

Figure 2

Proposed mechanism of food with pro- and antioxidant properties in the development of PD. Description of how the excessive intake of oxidized proteins and lipids causes the synthesis of oxidized molecules that worsens the symptoms of PD. A diet rich in carbohydrates can increase oxidative stress and cause oxidative neuronal damage. Food products can help to neutralize mediators of PD progression.