A lively dinner discussion with a few biochemists on an article titled “Oxidative Stress and its Downstream Signaling in Aging Eyes” recently published in Clinical Intervention in Aging spurred today’s Friday Pearl on oxidative stress.
Oxidative stress is the biochemical end point of the imbalance between reactive oxygen species (ROS) production and the ability of nutrient-based antioxidants to fight against oxidative injury, including in the eye.
Clinical, biochemical and molecular data from anterior and posterior eye segment diseases point to oxidative stress as the common pathogenic mechanism in the majority of ocular disorders including pathologies causing visual impairment, blindness, and loss of quality of life.
Nutritional supplement studies strongly suggest that well-designed full-spectrum supplements should be considered standard-of-care for all patients in order to best manage the aging population including those with ocular diseases.
All biomolecules can be attacked by reactive oxygen species including lipids, proteins and nucleic acids; with lipids, including essential fatty acids, being the most susceptible to oxidation, particularly those ingested without protective antioxidants as part of the meal or supplement.
Our cells maintain a healthy environment through the production of metabolizing enzymes and a consistent supply of metabolic energy. The amount of detrimental oxidative stress effect is dependent on the optimal production of energy and the supply of micronutrients necessary to produce it.
When cells and their membranes do not have enough ongoing antioxidant protection they are too frequently unable to overcome excessive oxidative stress, or to recover optimal cellular function.
The introduction of antioxidant defenses after the fact, frequently cannot counter the effect of reactive oxygen species (think closing the barn door after the horse escapes).
Knowing something about metabolic pathways that regulate reactive oxygen homeostasis is pivotal for relieving the deleterious effects of reactive oxygen in cells and tissues, particularly where the aging process is concerned, which is a continuous, complex, and dynamic process that begins with birth and ends with death.
One of the best known antioxidant defense system is the mineral-based molecular enzyme, superoxide dismutase copper, zinc SOD (CuZnSOD), which was discovered in 1969 to participate in intracellular pathogenic mechanisms of a number of diseases including atherosclerosis, Parkinson’s and Alzheimer’s, as well as ocular surface disorders, cataracts, glaucoma, diabetic retinopathy, uveitis and age-related macular degeneration.
Unfortunately, molecular manganese superoxide dismutase enzyme (MnSOD) is required to support cellular mitochondrial antioxidant activity in the human, particularly in the eye and brain, and it has been virtually overlooked in most ocular-focused nutritional eye disease studies.
Again, and again—it makes biological sense that we cannot and should not fragment nutrition and expect great long-term nutrient study results.
Free radical nutrient-based scavengers slow down the reactions of oxidation, transforming them into less aggressive compounds. They are hydro soluble and cytosolic glutathione and vitamin C, or liposolubles, vitamins E and carotenoids.
Vitamin C regenerates vitamin E, which is one of the main liposoluble antioxidants in cellular membranes, together with the carotenoids, including hydro-carbon lutein and the xanthophyll carotenoids, zeaxanthin and mesozeaxanthin.
This is a great place to introduce a biological sound suggestion: always make sure the fish oil you are consuming includes stabilizing liposoluble antioxidants, which are necessary to help prevent cellular membrane oxidative stress leading to the inability of membranes to efficiently move nutrients into the cell and mitochondrial waste byproducts out of the cell.
The flavonoids (rutin and quercetin) are also too often overlooked in nutritional supplements designed for the eye and brain. These molecules chelate (bind) excessive iron and copper, preventing Fenton reactions and the formations of destructive lipid peroxide radicals.
Via: Ellen Troyer, with Spencer Thornton, MD and the Biosyntrx staff
PEARL: The gain in life-span has been far greater in many other countries than in the United States. We now rank thirty fifth in longevity, which suggests that older people in our country may be suffering earlier age-related chronic diseases than populations in a large number of other industrialized countries.
Environment and lifestyle choices affect concentration of endogenous antioxidants during the aging process, so obviously, reactive oxygen species production increases with our earlier aging process.
It’s clear that individual lifestyle choices are playing an important role in our health, our aging process and the enormous cost of healthcare, which can be changed through improved personal responsibility for dietary intake, supplements and exercise.
References for this column, plus a surgical instrument announcement from our friends at Crestpoint Management can be found here.