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Micronutrients
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Vitamin C, also known as L-ascorbic acid or ascorbate, is a water-soluble vitamin, an important essential micronutrient for the human body and a co-factor in at least eight enzymatic reactions in humans. Vitamin C is a six-carbon lactone; a simple sugar with molecular weight of 176 Da. It is synthesized from glucose by many plants and animals. Vitamin C is synthesized in the liver in most mammals and in the kidney in birds and reptiles. However, some vertebrate species: humans, teleost fishes, guinea pigs, bats and some primates such as monkeys, simians and tarsiers are unable to synthesize vitamin C because they lack an enzyme named gulonolactone oxidase used for the conversion of glucose to vitamin C (3, 9, 33, 48–51). Humans lost this capability to synthesize vitamin C endogenously, about 40 million years ago, due to the development of mutations in the gulonolactone oxidase gene leading to stop the vitamin C biosynthetic pathway (49–50). Therefore, the provision of vitamin C via foods is vital for human life. Acute lack of vitamin C leads to scurvy, a disease characterized by blood vessel fragility, connective tissue damage, fatigue, and ultimately, death as result of a general collapse (3, 9, 23, 33, 48–54). As humans cannot obtain this vitamin endogenously, different artificial L-ascorbic acid syntheses have been developed by a combined chemical and microbial method for the production of L-ascorbic acid from D-glucose (55).
Ascorbate and the Hypoxic Response in Cancer
Published in Qi Chen, Margreet C.M. Vissers, Cancer and Vitamin C, 2020
Christina Wohlrab, Caroline Kuiper, Gabi U. Dachs
Vitamin C (ascorbate) is an essential micronutrient for humans and must be acquired via our diet. Humans are unable to synthesize ascorbate due to mutations in gulonolactone oxidase (GULO), the terminal enzyme of the biosynthesis pathway [1]. Although our absolute requirement for this vitamin has long been established, its many roles in health and disease, and its mechanisms of action, are only now being uncovered. Here we describe how ascorbate may affect cancer progression via modulation of the hypoxic response pathway.
Vitamin C Pharmacokinetics *
Published in Qi Chen, Margreet C.M. Vissers, Vitamin C, 2020
The enzyme L-gulonolactone oxidase catalyzes the final step in the biosynthesis of ascorbic acid in almost all vertebrates [1]. However, evolutionally conserved deletions have rendered the corresponding gene inactive or lost in primates and a few other species, making us dependent on ingestion of vitamin C [1]. Although not investigated in full detail, some evidence suggests that the same evolutionary process has also adapted humans and other vitamin C–dependent species to this dependency by altering their pharmacokinetic handling of vitamin C, that is, improving the ability to take up and recycle vitamin C while limiting its excretion for optimal health [2,3].
Climatic Droplet Keratopathy Is a Misnomer for This Corneal Degeneration
Published in Seminars in Ophthalmology, 2023
Horacio M. Serra, Pablo A. Moro
Ultraviolet radiation (UVR) is absorbed by the cornea differentially based on the incident wavelength. Ultraviolet B (UVB) can damage the cornea through the generation of free radicals, lipid peroxidation, and DNA fragmentation. The eye is one of the major targets of reactive oxygen species (ROS) and reactive nitrogen species (RNS) attack due to hazardous exposure to UVR and environmental factors such as high oxygen pressure, ionizing radiation, chemical pollutants, and pathogenic microbes, which can shift the redox status of a cell towards oxidizing conditions. Lipid peroxidation is initiated when ROS attacks polyunsaturated fatty acids chains in cell membrane phospholipids and may cause the accumulation of reactive aldehydes. Unlike ROS, aldehydes are generally long-lived compounds that can diffuse through the cell. The protective mechanisms against these attacks are mediated by ascorbic acid (AA, or vitamin C), aldehyde dehydrogenases (ALDHs), and glutathione peroxidase.51,52 AA is synthesized from glucose in the organism of some animals through an enzymatic process that involves the enzyme L-gulonolactone oxidase. This enzyme is absent in humans, Guinea pigs, and some varieties of bats and birds, so all of them need to eat food containing AA to avoid a deficit of this vitamin. Despite these defenses, there is increasing evidence indicating that oxidative stress plays an important role in the development of many ocular diseases.53
The interaction between vitamin C and bone health: a narrative review
Published in Expert Review of Precision Medicine and Drug Development, 2018
Alberto Falchetti, Roberta Cosso
At physiological pH, the ascorbate monoanion is the dominant form of vitamin C (99%) followed by ASC and the ascorbate dianion in very low concentrations (0.005%) (Figure 2). At acid pH, ASC is the main molecular form [4–7]. Vitamin C is synthesized from glucose (d-glucuronic acid) in most animals (Figure 3). However, humans and other primates are not able to synthesize vitamin C, because the gene encoding l-gulonolactone oxidase, the last enzyme in ascorbate synthesis, is not functional, probably because of a mutation appeared over 40 million years ago. Standard belief among scientists is that the GULO gene could have been ‘prepared’ to be lost/changed (pseudo-gene) versus other genes, since it produces an enzyme, presumably, not working in other biochemical pathways. However, some questions are still waiting for a clear answer: (1) Since scurvy is fatal, why GULO gene mutation has not been deleted?; (2) Why the consequences of this mutation have not been rapid and fatal?; and (3) Did the mutation occur in a population of mammals with high intakes of vitamin C in the diet? It would have had no consequence in such a population.