ROS, Anthocyanins and Diseases

Daily, the human body is affected by stress, pollution, unbalanced nutrition and other internal and external factors that can alter the body metabolism, thus creating a pathway to pathogens and diseases. An unbalanced metabolism generates free radicals (or reactive oxygen species – ROS), which attack biological macromolecules in the human body such as proteins, fatty acids and DNA. When free radicals are in great numbers in the human body, they cause oxidative stress, causing damage on cells, tissues or even gene mutation.

The human body is constantly fighting pathogens with the help of white blood cells, or anti-bodies. The cells, on their own turn, also have their own defense system, which prevents cell invasion by external threats, such as viruses, but that also helps to fix any DNA alterations (mutations), which can be passed on to the daughter cells during cell division. However, when free radicals are in high concentration in the human body, they cause oxidative damage to cells, thus destroying internal reduction-oxidation balance (the capacity of cells to eliminate a faulty gene and to cause apoptosis or programed cell death – PCD). Oxidative stress is linked to causing a variety of ailments, even premature aging[1]. Recent studies have proven that several of the diseases that haunt modern society are linked to free radicals and oxidative stress, including arteriosclerosis, diabetes, cataract, cardiovascular diseases, Parkinson’s disease, Alzheimer’s dis-ease and arthritis[2].

The consumption of antioxidants is necessary in order for cells to be protected from free radicals’ attack; therefore, to prevent and treat several diseases. The best antioxidants for human consumption are those of natural origin (such as anthocyanins found in New Zealand Blackcurrants as well as in other fruits), as they not only help the human body maintain the balance of homeostasis but also, they do not have toxins that may cause adverse reaction, something normally linked to synthetic antioxidants[3].

Health Habits and ROS

ROS include free radicals that are formed by the stepwise reduction of molecular oxygen (O2) by high-energy exposure or electro transfer reactions. The exposure of the human body to pollution, stress, unhealthy diets and even pesticides can trigger the formation of ROS. All ROS are extremely harmful to organisms at high concentrations. When levels of ROS exceed the defense mechanisms, a cell is said to be in a state of “oxidative stress”. The enhanced production of ROS because of daily behaviors (e.g. smoking) can pose a threat to cells by causing peroxidation of lipids, oxidation of proteins, damage to nucleic acids, enzyme inhibition, activation of programed cell death (PCD) pathway and ultimately leading to death of the cells. However, ROS do not only have a destructive activity.  They play important roles in the modulation of cell survival, cell death, differentiation, cell signaling, and inflammation-related factor production (Dayem et al. 2017). ROS become toxic to the cells when their concentration increases to the point of causing oxidative injury and they are not eliminated from the body completely. A balance between ROS production and scavenging (or detoxification) is achieved by an efficient antioxidative system inside the cells comprising of enzymic and nonenzymic antioxidants, regulated by various detoxifying enzymes, such as SOD, glutathione peroxidase (GPX), and catalase (CAT), or by different antioxidants, including flavonoids, ascorbic acids, vitamin E, and glutathione (GSH). [4],[5],[6]

The Use of Anthocyanins in the Prevention of Diseases and Inflammation

Several studies have shown the connection between oxidative stress and diseases, since an unbalanced redox homeostasis can directly reduce the cells’ capacity to defense themselves from pathogens. Oxidative stress also breaks the cells’ ability to either detect a faulty gene and fix it, or to prevent the mutation from multiplying in the human body through cell division[7],[8]. Conversely, antioxidants inhibit the proliferation of faulty cells[9]. ATM (ataxia telangiectasia mutated) is one of the proteins involved in cell cycle regulation that are activated by ROS. Patients lacking ATM show higher levels of oxidative damage and similar effects in obtained with ATM knockout mice can be rescued with administration of antioxidants[10]. Altogether, this suggests ROS as positive regulators of inflammation by modulating key.

Proteins in cell cycle progression. With diseases such as arthritis, more nascent blood vessels are developed to facilitate oxygen and nutrient supply to the center of the inflammation[11]. Although this is a natural response to fight inflammation in any part of the body, blood flow to the sick area(s) is usually problematic due to vasoconstriction caused by the inflammation. Poor circulation causes hypoxia (low oxygen levels), which then leads to further oxidative stress[12]. Contrarily to ROS, antioxidants mediate the increase in ROS concentration in the body and protect human cells and tissues; thus, treating and preventing diseases and inflammation. New Zealand blackcurrants are even more advantageous in combating certain ailments and inflammatory processes because they are plant-based, as in they are free from toxins that normally are present in synthetic antioxidants. Furthermore, there are literally hundreds of scientific researches that have either been carried out or are under way that prove the wonderful health benefits of a balanced, nutritious diet and daily consumption of anthocyanin-rich New Zealand blackcurrant.


Copyright © 2017 Vitality® New Zealand




[1] R.K. Gupta, A.K. Patel, N. Shah, et al., Oxidative stress and antioxidants in disease and cancer: a review, Asian Pac. J. Cancer Prev. 15 (2014) 4405–4409.
[2] J. Labat-Robert, L. Robert, Longevity and aging. Role of free radicals and xanthine oxidase. A review, Pathol. Biol. (Paris) 62 (2014) 61–66.
[3] Li, Guowei Chen, Chao Zhang, Man Wu, et al., Research progress of natural antioxidants in foods for the treatment of diseases. Food Science and Human Wellness 3 (2014) 110–116.
[4] Wu, H.; Yin, J.-J.; Wamer, W.G.; Zeng, M.; Lo, Y.M. Reactive oxygen species-related activities of nano-iron metal and nano-iron oxides. J. Food Drug Anal. 2014, 22, 86–94.
[5] Halliwell, B.; Clement, M.V.; Long, L.H. Hydrogen peroxide in the human body. FEBS Lett. 2000, 486, 10–13.
[6] Hampton, M.B.; Orrenius, S. Dual regulation of caspase activity by hydrogen peroxide: Implications for apoptosis. FEBS Lett. 1997, 414, 552–556.
[7] Storz P. Reactive oxygen species in tumor progression. Front Biosci. 2005;10:1881–96. Szatrowski TP, Nathan CF. Production of large amounts of hydrogen peroxide by human tumor cells. Cancer Res. 1991;51(3):794–8. Gupta A, Rosenberger SF, Bowden GT. Increased ROS levels contribute to elevated transcription factor and MAP kinase activities in malignantly progressed mouse keratinocyte cell lines. Carcinogenesis. 1999;20(11):2063–73.
[8] Storz P. Reactive oxygen species in tumor progression. Front Biosci. 2005;10:1881–96. Burdon RH, Gill V, Rice-Evans C. Oxidative stress and tumour cell proliferation. Free Radic Res Commun. 1990;11(1–3):65–76.
[9] Behrend L, Henderson G, Zwacka RM. Reactive oxygen species in oncogenic transformation. Biochem Soc Trans. 2003;31(Pt 6):1441–4.
[10] Browne SE, et al. Treatment with a catalytic antioxidant corrects the neurobehavioral defect in ataxia-telangiectasiamice. Free Radic Biol Med. 2004;36(7):938–42. Reichenbach J, et al. Elevated oxidative stress in patients with ataxia telangiectasia. Antioxid Redox Signal. 2002;4(3):465–9.
[11] Claffey KP, et al. Expression of vascular permeability factor/vascular endothelial growth factor by melanoma cells increases tumor growth, angiogenesis, and experimental metastasis. Cancer Res. 1996;56(1):172–81. Senger DR, et al. Vascular permeability factor, tumor angiogenesis and stroma generation. Invasion Metastasis. 1994;14(1–6):385–94.
[12] Brown NS, Bicknell R. Hypoxia and oxidative stress in breast cancer. Oxidative stress: its effects on the growth, metastatic potential and response to therapy of breast cancer. Breast Cancer Res. 2001;3(5):323–7.