The identification of homocystine in the urine

Gerritsen, Theo; Vaughn, James G.; Waisman, Harry A.

doi:10.1016/0006-291x(62)90114-6

Cited by 251 publications

(69 citation statements)

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“…First described in 1962 in a cohort of patients with mental retardation, 45 homocystinuria is the result of impairment of the methionine synthesis pathway. Major clinical manifestations affect the central nervous, vascular and skeletal systems.…”

Section: Homocystinuria and Hypomethionemiamentioning

confidence: 99%

Investigation of inter-individual variability of the one-carbon folate pathway: a bioinformatic and genetic review

2009

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Section: Homocystinuria and Hypomethionemiamentioning

confidence: 99%

Investigation of inter-individual variability of the one-carbon folate pathway: a bioinformatic and genetic review

2009

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“…Individuals who consume a large amount of food rich in animal protein may ingest two to three grams of methionine, resulting in postprandial Hcy concentrations greater than 20 µmol/L. Clinical HHcy was first described more than 40 years ago in children with learning difficulties [1][2][3] , and it has since been estimated that moderate HHcy occurs in 5-7% of the general population. Evidence now indicates that moderate HHcy is an important and independent risk factor for several disorders, including atherosclerosis, diabetes, fatty liver, immune activation, and neurodegenerations such as Alzheimer's and Parkinson's diseases [3][4][5][6][7][8][9] .…”

Section: Introductionmentioning

confidence: 99%

Hyperhomocysteinemia, endoplasmic reticulum stress, and alcoholic liver injury

Cheng

Kaplowitz

2004

WJG

179

104

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Deficiencies in vitamins or other factors (B6, B12, folic acid, betaine) and genetic disorders for the metabolism of the non-protein amino acid-homocysteine (Hcy) lead to hyperhomocysteinemia (HHcy). HHcy is an integral component of several disorders including cardiovascular disease, neurodegeneration, diabetes and alcoholic liver disease. HHcy unleashes mediators of inflammation such as NFκB, IL-1β, IL-6, and IL-8, increases production of intracellular superoxide anion causing oxidative stress and reducing intracellular level of nitric oxide (NO), and induces endoplasmic reticulum (ER) stress which can explain many processes of Hcy-promoted cell injury such as apoptosis, fat accumulation, and inflammation. Animal models have played an important role in determining the biological effects of HHcy. ER stress may also be involved in other liver diseases such as α 1 -antitrypsin (α 1 -AT) deficiency and hepatitis C and/or B virus infection. Future research should evaluate the possible potentiative effects of alcohol and hepatic virus infection on ER stress-induced liver injury, study potentially beneficial effects of lowering Hcy and preventing ER stress in alcoholic humans, and examine polymorphism of Hcy metabolizing enzymes as potential risk-factors for the development of HHcy and liver disease. Ji C, Kaplowitz N. Hyperhomocysteinemia, endoplasmic reticulum stress, and alcoholic liver injury.

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“…The more you smoke, the greater your risk [17][18][19][20][21][22][23][24][25]. We show that from our cross sectional study that the results in the volunteers is slightly higher in males than in females.…”

Section: Discussionmentioning

confidence: 63%

Effect of Smoking Index on Cardiovascular System in Some Libyans

2017

ARC Journal of Forensic Science

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The identification of homocystine in the urine

Cited by 251 publications

References 3 publications

Investigation of inter-individual variability of the one-carbon folate pathway: a bioinformatic and genetic review

Investigation of inter-individual variability of the one-carbon folate pathway: a bioinformatic and genetic review

Hyperhomocysteinemia, endoplasmic reticulum stress, and alcoholic liver injury

Effect of Smoking Index on Cardiovascular System in Some Libyans

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