ALDH3A1

ALDH3A1

A gene on chromosome 17p11.2 that encodes an aldehyde dehydrogenase that plays a major role in detoxifying alcohol-derived acetaldehyde, metabolising corticosteroids, biogenic amines, neurotransmitters and in lipid peroxidation. The ALDH3A1 gene product forms a homodimer that preferentially oxidises aromatic and medium-chain (6 carbons or more) saturated and unsaturated aldehyde substrates. It appears to promote resistance to UV light-induced oxidative damage in the cornea.

Molecular pathology
ALDH3A1 mutation may cause Smith-Magenis syndrome.
References in periodicals archive ?
Finally, the Gene Set Enrichment Analysis showed that several tumorigenesis-related genes were enriched in the "colon CTC signature," such as carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5) and carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6), phospholipase A2 group 2A (PLA2G2A), and aldehyde dehydrogenase 3 family member A1 (ALDH3A1).
Finally, this AHR-dependent pathway has target genes such as CYP1A1, CYP1A2, and CYP1B1 and aldehyde dehydrogenase 3A1 (ALDH3A1) [30,31].
The following are phase I enzymes: cytochrome P450 1 subfamily (Cyp1a1, Cyp1a2, and Cyp1b1) and aldehyde dehydrogenase 3A1 (Aldh3a1) as a participant of phase II of the xenobiotic metabolism [16].
TRI-Reagent and RNA Secure Reagent were purchased from Ambion (USA); the cDNA synthesis MMLV RT kit and PCR kit qPCRmix-HS were from Evrogen (Russia); RNasin and RQ1 DNase were from Promega (USA); oligonucleotides (primers) for analysis of the rat genes Cyp1a1, Cyp1a2, Cyp1b1, Gsta1, Nqo1, Aldh3a1, Ugt1a6, Ugt1a9, AhR, Nrf2, Gsr, Txnrd1, Hmox1, and Gapdh were from Syntol (Russia).
Figure 1 shows mRNA levels of AhR and AhR-dependent genes of phase I (Cyp1a1, Cyp1a2, and Cyp1b1) and phase II (Aldh3a1).
According to two-way ANOVA there were no statistically significant differences in the mRNA expression of Aldh3a1 (Figure 1(c)) either between the 2 strains ([F.sub.1,25] =3.7, P = 0.07) or between SkQ1 supplementation and control ([F.sub.1,25] = 2.5, P = 0.13).
Vasiliou, "ALDH3A1 protects human corneal epithelial cells from ultraviolet- and 4-hydroxy-2-nonenal-induced oxidative damage," Free Radical Biology and Medicine, vol.
The corneal epithelial cells accumulate high levels of taxon-specific corneal crystallins aldehyde dehydrogenase 3A1 (Aldh3a1) and transketolase (Tkt), which account for about 50% and 10% of water-soluble proteins, respectively [9-11], along with structural proteins such as keratin-12 [12].
Direct involvement of Klf4 has been demonstrated in regulation of corneal epithelial expression of keratin-12, aquaporin-3, aquaporin-5, and corneal crystallins TKT and Aldh3a1 [65, 66].
However, posttranscriptional regulation appears to play a significant role in the expression of corneal crystallins aldehyde dehydrogenase IIIA1 (Aldh3a1) and transketolase (Tkt), which constitute roughly 50% and 10% of the water-soluble protein, respectively, and only about 1% each of the total mRNA in the adult cornea [31].
The corneal crystallin Aldh3a1 is expressed at about 500-fold higher level in the mouse corneal epithelial cells than in other tissues [231].
We a priori designated a "high-risk" allele for each polymorphism based on the expected functional impact with respect to acetylcholinesterase (AChE) inhibition (OP and carbamate insecticides; PON1, BCHE, FMO1, FM03, and GSTT1 polymorphisms) and ion channel stimulation [OC and pyrethroid insecticides; aldehyde dehydrogenase 3A1 (ALDH3A1) and GSTT1 polymorphisms].