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      Methylenetetrahydrofolate reductase C677T variant and hyperhomocysteinemia in subarachnoid hemorrhage patients from India

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          Most cited references49

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          Purification of nucleic acids by extraction with phenol:chloroform.

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            Is Open Access

            The Molecular and Cellular Effect of Homocysteine Metabolism Imbalance on Human Health

            Homocysteine (Hcy) is a sulfur-containing non-proteinogenic amino acid derived in methionine metabolism. The increased level of Hcy in plasma, hyperhomocysteinemia, is considered to be an independent risk factor for cardio and cerebrovascular diseases. However, it is still not clear if Hcy is a marker or a causative agent of diseases. More and more research data suggest that Hcy is an important indicator for overall health status. This review represents the current understanding of molecular mechanism of Hcy metabolism and its link to hyperhomocysteinemia-related pathologies in humans. The aberrant Hcy metabolism could lead to the redox imbalance and oxidative stress resulting in elevated protein, nucleic acid and carbohydrate oxidation and lipoperoxidation, products known to be involved in cytotoxicity. Additionally, we examine the role of Hcy in thiolation of proteins, which results in their molecular and functional modifications. We also highlight the relationship between the imbalance in Hcy metabolism and pathogenesis of diseases, such as cardiovascular diseases, neurological and psychiatric disorders, chronic kidney disease, bone tissue damages, gastrointestinal disorders, cancer, and congenital defects.
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              Geographical and ethnic variation of the 677C>T allele of 5,10 methylenetetrahydrofolate reductase (MTHFR): findings from over 7000 newborns from 16 areas world wide.

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                Author and article information

                Journal
                Metabolic Brain Disease
                Metab Brain Dis
                Springer Science and Business Media LLC
                0885-7490
                1573-7365
                October 2018
                June 21 2018
                October 2018
                : 33
                : 5
                : 1617-1624
                Article
                10.1007/s11011-018-0268-5
                29926428
                120b68c9-b857-4e5d-b504-5f596bb6af2d
                © 2018

                http://www.springer.com/tdm

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