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Table 1 Comparison between ALDH1A1 and ALDH2, in terms of expression, biochemistry and PD-related aspects

From: Impaired dopamine metabolism in Parkinson’s disease pathogenesis

  ALDH1A1 ALDH2
Tissue expression Brain, eye lens, retina, lung, liver, kidney, testis [104] Liver, kidney, heart, lung, brain [104]
Subcellular localization Cytosol [40, 105, 106] Mitochondrial matrix [104]
Substrates Retinaldehyde (km < 0.1 μM) [116]
DOPAL (km 0.4 μM) [24, 113, 114]
4-HNE (km 4.8 μM [117]; 17.9 μM [118])
MDA (km 3.5 μM [117]; 114.4 μM [119])
Ƴ-aminobutyraldehyde (800 μM) [112]
Acetaldehyde (km < 1 μM) [120]
DOPAL (km 1 μM) [121]
4-HNE and MDA [122,123,124]
Ƴ-aminobutyraldehyde (500 μM) [112]
PD-related   
Genetic variants N.A - Haplotype: rs737280; rs968529; rs16941667; rs16941669; rs9971942 (California) [125]
- Haplotype: rs4767944; rs441; rs671 (China) [126]
- rs671 SNP (China) [127]
Expression levels Reduced mRNA levels:
- TH-positive neurons in PD patients’ brain [128]
- transgenic A53T mouse striatum [129]
N.A.
Decreased protein levels:
- PD patients’ brain [130, 131]
-LRRK2-G2019S knock-in mouse DA neurons [132]
Enzyme inhibition * Epidemiological studies:
- traces of Dieldrin in tissues of exposed PD patients [133]
- Benomyl exposure correlates with PD risk [134]
In vitro:
- 4-HNE and MDA [135, 136]
- DOPAL (> 5 μM) [121, 136]
- Benomyl [134]
Cellular models of ALDH inhibition:
- rat purified synaptosomes treated with 4-HNE and MDA [34]
- SH-SY5Y cells treated with Disulfiram [137]
- Neurons from Daidzin administered hamster [138]
- PC6–3 cells treated with Dieldrin [139]
- primary neurons and SK-N-MC cells treated with Benomyl [134]
In vivo models * Genetic models:
- A53T/Aldh1a1−/−mouse [40]
- Aldh1a1−/−/Aldh2−/− mouse [28]
- Aldh1a1−/−/Gpx−/− mouse [140]
Toxin-based models:
- Benomyl intraperitoneally administered mouse [141]
- Benomyl exposed zebrafish embryos [134]
- Ziram exposed zebrafish embryos [142]
  1. *The “Enzyme Inhibition” and “In vivo models” sections refer to both ALDH1A1 and ALDH2
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