PMID- 29532755
OWN - NLM
STAT- MEDLINE
DCOM- 20191028
LR  - 20191028
IS  - 1875-533X (Electronic)
IS  - 0929-8673 (Linking)
VI  - 26
IP  - 16
DP  - 2019
TI  - Homocysteine and Hyperhomocysteinaemia.
PG  - 2948-2961
LID - 10.2174/0929867325666180313105949 [doi]
AB  - Homocysteine (Hcy) is a thiol group containing the amino acid, which naturally 
      occurs in all humans. Hcy is degraded in the body through two metabolic pathways, 
      while a minor part is excreted through kidneys. The chemical reactions that are 
      necessary for degradation of Hcy require the presence of folic acid, vitamins B6 
      and B12. Consequently, the level of the total Hcy in the serum is influenced by 
      the presence or absence of these vitamins. An elevated level of the Hcy, 
      hyperhomocysteinemia (HHcy) and homocystinuria is connected with occlusive artery 
      disease, especially in the brain, the heart, and the kidney, in addition to 
      venous thrombosis, chronic renal failure, megaloblastic anemia, osteoporosis, 
      depression, Alzheimer's disease, pregnancy problems, and others. Elevated Hcy 
      levels are connected with various pathologies both in adult and child population. 
      Causes of HHcy include genetic mutations and enzyme deficiencies in 5, 
      10-methylenetetrahydrofolate reductase (MTHFR) methionine synthase (MS), and 
      cystathionine beta-synthase (CbetaS). HHcy can be caused by deficiencies in the folate, 
      vitamin B12 and to a lesser extent, deficiency in B6 vitamin what influences 
      methionine metabolism. Additionally, HHcy can be caused by the rich diet and 
      renal impairment. This review presents literature data from recent research 
      related to Hcy metabolism and the etiology of the Hcy blood level disorder. In 
      addition, we also described various pathological mechanisms induced by hereditary 
      disturbances or nutritional influences and their association with HHcy induced 
      pathology in adults and children and treatment of these metabolic disorders.
CI  - Copyright(c) Bentham Science Publishers; For any queries, please email at 
      epub@benthamscience.net.
FAU - Zaric, Bozidarka L
AU  - Zaric BL
AD  - Institute of nuclear science Vinca, University of Belgrade, Laboratory of 
      Radiobiology and Molecular Genetics, Belgrade, Serbia.
FAU - Obradovic, Milan
AU  - Obradovic M
AD  - Institute of nuclear science Vinca, University of Belgrade, Laboratory of 
      Radiobiology and Molecular Genetics, Belgrade, Serbia.
FAU - Bajic, Vladan
AU  - Bajic V
AD  - Institute of nuclear science Vinca, University of Belgrade, Laboratory of 
      Radiobiology and Molecular Genetics, Belgrade, Serbia.
FAU - Haidara, Mohamed A
AU  - Haidara MA
AD  - Department of Physiology, College of Medicine, King Khalid University, Abha, 
      Saudi Arabia.
FAU - Jovanovic, Milos
AU  - Jovanovic M
AD  - Faculty of Biology, University of Belgrade, Institute of physiology and 
      biochemistry, Belgrade, Serbia.
FAU - Isenovic, Esma R
AU  - Isenovic ER
AD  - Institute of nuclear science Vinca, University of Belgrade, Laboratory of 
      Radiobiology and Molecular Genetics, Belgrade, Serbia.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United Arab Emirates
TA  - Curr Med Chem
JT  - Current medicinal chemistry
JID - 9440157
RN  - 0LVT1QZ0BA (Homocysteine)
RN  - 8059-24-3 (Vitamin B 6)
RN  - 935E97BOY8 (Folic Acid)
RN  - EC 1.5.1.20 (Methylenetetrahydrofolate Reductase (NADPH2))
RN  - EC 2.1.1.13 (5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase)
RN  - EC 4.2.1.22 (Cystathionine beta-Synthase)
RN  - P6YC3EG204 (Vitamin B 12)
SB  - IM
MH  - 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase/deficiency/genetics
MH  - Animals
MH  - Avitaminosis
MH  - Cystathionine beta-Synthase/deficiency/genetics
MH  - Folic Acid/therapeutic use
MH  - Homocysteine/*metabolism
MH  - Humans
MH  - Hyperhomocysteinemia/drug therapy/*etiology/genetics
MH  - Methylenetetrahydrofolate Reductase (NADPH2)/deficiency/genetics
MH  - Vitamin B 12/therapeutic use
MH  - Vitamin B 6/therapeutic use
OTO - NOTNLM
OT  - Homocysteine
OT  - cardiovascular diseases
OT  - disturbance of homocysteine metabolism
OT  - homocysteine metabolism
OT  - hyperhomocysteinemia
OT  - nutritional deficiencies.
EDAT- 2018/03/14 06:00
MHDA- 2019/10/29 06:00
CRDT- 2018/03/14 06:00
PHST- 2017/09/04 00:00 [received]
PHST- 2018/01/03 00:00 [revised]
PHST- 2018/03/05 00:00 [accepted]
PHST- 2018/03/14 06:00 [pubmed]
PHST- 2019/10/29 06:00 [medline]
PHST- 2018/03/14 06:00 [entrez]
AID - CMC-EPUB-89062 [pii]
AID - 10.2174/0929867325666180313105949 [doi]
PST - ppublish
SO  - Curr Med Chem. 2019;26(16):2948-2961. doi: 10.2174/0929867325666180313105949.