Assessment of the relationship between the antimutagenic action of riboflavin and glutathione and the levels of antioxidant enzymes

Durusoy, Mübeccel; Karagöz, Emel; Öztürk, Kamile

doi:10.1016/s0955-2863(02)00207-3

Cited by 9 publications

(6 citation statements)

References 17 publications

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“…Brain cells are particularly susceptible to oxidative stress due to their higher metabolic activity and lower antioxidant activity, compared to many cells of other organs, suggesting that redox metabolism may be an important factor for neuronal death. There are several plausible models proposing how riboflavin could protect cells against oxidative stress by: (1) enhancing the glutathione redox cycle 60 , (2) deactivating the lipid peroxides 61 , (3) direct activity against free radicals 62 , and (4) enhancing antioxidant enzyme activities 63 . Oxidative stress is also often accompanied by mitochondrial dysfunction, which may exacerbate disease progression 64 and it was shown in several case studies that riboflavin administration in patients with mitochondrial diseases can lead to clinical improvement 65,66 .…”

Section: Discussionmentioning

confidence: 99%

FMN reduces Amyloid-β toxicity in yeast by regulating redox status and cellular metabolism

Chen

Hao

et al. 2020

Nat Commun

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Alzheimer's disease (AD) is defined by progressive neurodegeneration, with oligomerization and aggregation of amyloid-β peptides (Aβ) playing a pivotal role in its pathogenesis. In recent years, the yeast Saccharomyces cerevisiae has been successfully used to clarify the roles of different human proteins involved in neurodegeneration. Here, we report a genome-wide synthetic genetic interaction array to identify toxicity modifiers of Aβ42, using yeast as the model organism. We find that FMN1, the gene encoding riboflavin kinase, and its metabolic product flavin mononucleotide (FMN) reduce Aβ42 toxicity. Classic experimental analyses combined with RNAseq show the effects of FMN supplementation to include reducing misfolded protein load, altering cellular metabolism, increasing NADH/(NADH + NAD +) and NADPH/(NADPH + NADP +) ratios and increasing resistance to oxidative stress. Additionally, FMN supplementation modifies Htt103QP toxicity and α-synuclein toxicity in the humanized yeast. Our findings offer insights for reducing cytotoxicity of Aβ42, and potentially other misfolded proteins, via FMN-dependent cellular pathways.

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Section: Discussionmentioning

confidence: 99%

FMN reduces Amyloid-β toxicity in yeast by regulating redox status and cellular metabolism

Chen

Hao

et al. 2020

Nat Commun

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“…Also, riboflavin has been suggested to have a direct activity against mutagen produced free radicals (35). Indeed, the protection of hepatocytes against reperfusion injury, in a state of ischemic liver, has been attributed to the independent antioxidant property of riboflavin (36).…”

Section: Riboflavin Ameliorates Oxidative Stress Mitochondrial Dysfumentioning

confidence: 99%

Riboflavin Has Neuroprotective Potential: Focus on Parkinson’s Disease and Migraine

Marashly

Bohlega

2017

Front. Neurol.

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With the huge negative impact of neurological disorders on patient’s life and society resources, the discovery of neuroprotective agents is critical and cost-effective. Neuroprotective agents can prevent and/or modify the course of neurological disorders. Despite being underestimated, riboflavin offers neuroprotective mechanisms. Significant pathogenesis-related mechanisms are shared by, but not restricted to, Parkinson’s disease (PD) and migraine headache. Those pathogenesis-related mechanisms can be tackled through riboflavin proposed neuroprotective mechanisms. In fact, it has been found that riboflavin ameliorates oxidative stress, mitochondrial dysfunction, neuroinflammation, and glutamate excitotoxicity; all of which take part in the pathogenesis of PD, migraine headache, and other neurological disorders. In addition, riboflavin-dependent enzymes have essential roles in pyridoxine activation, tryptophan-kynurenine pathway, and homocysteine metabolism. Indeed, pyridoxal phosphate, the active form of pyridoxine, has been found to have independent neuroprotective potential. Also, the produced kynurenines influence glutamate receptors and its consequent excitotoxicity. In addition, methylenetetrahydrofolate reductase requires riboflavin to ensure normal folate cycle influencing the methylation cycle and consequently homocysteine levels which have its own negative neurovascular consequences if accumulated. In conclusion, riboflavin is a potential neuroprotective agent affecting a wide range of neurological disorders exemplified by PD, a disorder of neurodegeneration, and migraine headache, a disorder of pain. In this article, we will emphasize the role of riboflavin in neuroprotection elaborating on its proposed neuroprotective mechanisms in opposite to the pathogenesis-related mechanisms involved in two common neurological disorders, PD and migraine headache, as well as, we encourage the clinical evaluation of riboflavin in PD and migraine headache patients in the future.

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“…It has been suggested that riboflavin may have antioxidant properties independent of its action in the glutathione redox cycle. Durusoy et al ( 46 ) reported that the antimutagenic effect of riboflavin is independent of antioxidant enzyme activity. They suggested that the antimutagenic effect of riboflavin can, at least in part, result from its direct scavenging activity on free radicals produced by mutagens.…”

Section: Effect Of Riboflavin Status On Lipid Peroxidationmentioning

confidence: 99%

Riboflavin (vitamin B₂) and oxidative stress: a review

2014

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Oxidative stress is involved in the development of many chronic diseases. One of the main factors involved in oxidative stress reduction is increased antioxidant potential. Some nutrients such as vitamin C, vitamin E and carotenoids are known to act as antioxidants; however, riboflavin is one of the neglected antioxidant nutrients that may have an antioxidant action independently or as a component of the glutathione redox cycle. Herein, studies that have examined the antioxidant properties of riboflavin and its effect on oxidative stress reduction are reviewed. The results of the reviewed studies confirm the antioxidant nature of riboflavin and indicate that this vitamin can protect the body against oxidative stress, especially lipid peroxidation and reperfusion oxidative injury. The mechanisms by which riboflavin protects the body against oxidative stress may be attributed to the glutathione redox cycle and also to other possible mechanisms such as the conversion of reduced riboflavin to the oxidised form.

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Assessment of the relationship between the antimutagenic action of riboflavin and glutathione and the levels of antioxidant enzymes

Cited by 9 publications

References 17 publications

FMN reduces Amyloid-β toxicity in yeast by regulating redox status and cellular metabolism

FMN reduces Amyloid-β toxicity in yeast by regulating redox status and cellular metabolism

Riboflavin Has Neuroprotective Potential: Focus on Parkinson’s Disease and Migraine

Riboflavin (vitamin B₂) and oxidative stress: a review

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Assessment of the relationship between the antimutagenic action of riboflavin and glutathione and the levels of antioxidant enzymes

Cited by 9 publications

References 17 publications

FMN reduces Amyloid-β toxicity in yeast by regulating redox status and cellular metabolism

FMN reduces Amyloid-β toxicity in yeast by regulating redox status and cellular metabolism

Riboflavin Has Neuroprotective Potential: Focus on Parkinson’s Disease and Migraine

Riboflavin (vitamin B2) and oxidative stress: a review

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Riboflavin (vitamin B₂) and oxidative stress: a review