Effects of Astaxanthin in the Central Nervous System

Oxidative stress is thought to be involved in the pathogenesis and progression of age-related cognitive impairments. The high lipid content and metabolic rate make the neuronal system particularly vulnerable to oxidative stress. Mitochondrial damage and dysfunction due to oxidative stress are reflected in age-related neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis.

In addition to metabolic failure, the membrane of the damaged mitochondria is impaired, their membrane potentials are lost, and they become permeable resulting in the release of cytochrome c. These processes lead to the activation of caspases that induce apoptosis of neuronal cells.

Dietary supplementation with antioxidant vitamins has shown preventive action against oxidative stress and protected or even reversed the age-related changes in antioxidant activity in the central nervous system. A recent review demonstrates that the systemic oxidative stress and the cognitive function in Alzheimer’s disease patients are inversely proportional. The administration of antioxidants, such as vitamin C or E, effectively reduces the symptoms of oxidative stress and cognitive loss.

Astaxanthin has recently gained a lot of interest because of its variety of health-promoting effects, mainly through modulating parameters related to oxidative stress and inflammation. Astaxanthin can penetrate the blood-brain barrier to accumulate in the brain and has positive effects on neurodegeneration.

The neuroprotective effect of astaxanthin was also published using in vitro and in vivo models. The 1-methyl-4-phenylpyridinium (MPP+) toxin was examined, which induces neuronal cytotoxicity. The oxidative stress evoked by this neurotoxin opens the mitochondrial permeability transition pore and subsequently triggers the release of cytochrome c.

Astaxanthin increases the activity of SOD and catalase, leading to the inhibition of MPP+-induced ROS generation. Astaxanthin seems to restore brain-derived neurotrophic factor (BDNF) levels in rats’ brains and hippocampus, thereby slowing brain aging.

The antineurotoxic effect of astaxanthin was also demonstrated an in vivo mouse model of Parkinson’s disease. A recent review summarizes further information on the potential neuroprotective role of astaxanthin.

Effects of Astaxanthin on the Skin

Age-related changes in the skin are thought to be driven by two basic mechanisms: biological aging and exposure to ultraviolet rays (photoaging). Photoaging leads to the degradation of components of the extracellular matrix (collagen, elastin), resulting in wrinkles, pigmentation, and deterioration of the skin texture. UV light initiates the production of ROS in the skin. Oxidation of C8 guanine base by ROS, 8-hydroxy-2deoxyguanosine (8-OHdG) is produced, a marker of DNA damage.

In keratinocytes and fibroblasts, ROS activate cytokine receptors and growth factors that will induce the mitogen-activated protein kinase (MAP kinase) and subsequently activate transcription factors of activator protein-1 (AP-1). AP-1 potentiates the expression of the matrix-degrading enzymes, the matrix metalloproteinases (MMPs), which impair collagen in the skin. Continuous carotenoid administration demonstrated protection against UV light. In particular, astaxanthin supplementation positively impacted aging skin status; the skin elasticity was restored, the wrinkle formation was attenuated, and epidermal barrier integrity was also restored.