Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (733 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Placing of a hydroxyl group on a compound in a position where one did not exist before. (Stedman, 26th ed)
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Hydroxylations.
Where it fits in the MeSH classification
- Broader topics
- Biochemical Phenomena; Organic Chemistry Phenomena; Metabolism
Research landscape
PubMed indexes 13,897 records tagged with the MeSH heading “Hydroxylation” (counts retrieved 2026-10-29). 1,079 of them (7.8%) were published from 2020 onward, and the busiest period so far is through 1999 with 6,836 records.
Reviews account for 750 records (5.4%) and meta-analyses for 1. Randomized controlled trials number 76 (0.5%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 6,836 |
| 2000-2009 | 2,881 |
| 2010-2019 | 3,101 |
| 2020 onward | 1,079 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 750 | 5.4% |
| Meta-analyses | 1 | 0.0% |
| Randomized controlled trials | 76 | 0.5% |
Method: PubMed query "Hydroxylation"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in molecular biology
Molecular biology establishes mechanisms through controlled experiments, often in simplified systems such as purified proteins, cultured cells or model organisms. Such work can show what is possible in a defined system, but whether a pathway matters in a whole organism or in human disease needs further evidence. Check the experimental system, whether findings were reproduced by independent groups, and whether the authors tested the mechanism directly or inferred it from correlation.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Differential effects of collagen prolyl 3-hydroxylation on skeletal tissues | 2014 | Research article Design not recorded in structured metadata | 31 | cc by PMID 24465224 · DOI · PMC3900401 |
| Bisphenol A Exposure and Sperm ACHE Hydroxymethylation in Men | 2019 | Research article Design not recorded in structured metadata | 19 | cc by PMID 30626059 · DOI · PMC6339044 |
| Hypoxia reduces the efficiency of elisidepsin by inhibiting hydroxylation and altering the structure of lipid rafts | 2013 | Research article Design not recorded in structured metadata | 11 | cc by PMID 24317474 · DOI · PMC3877891 |
Differential effects of collagen prolyl 3-hydroxylation on skeletal tissues [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Mutations in the genes encoding cartilage associated protein (CRTAP) and prolyl 3-hydroxylase 1 (P3H1 encoded by LEPRE1) were the first identified causes of recessive Osteogenesis Imperfecta (OI).
- Closing excerpt
- Our observations suggest differential tissue consequences due to selective inactivation of P3H1 hydroxylase activity versus complete ablation of the prolyl 3-hydroxylation complex.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (294 words)
Mutations in the genes encoding cartilage associated protein (CRTAP) and prolyl 3-hydroxylase 1 (P3H1 encoded by LEPRE1) were the first identified causes of recessive Osteogenesis Imperfecta (OI). These proteins, together with cyclophilin B (encoded by PPIB), form a complex that 3-hydroxylates a single proline residue on the α1(I) chain (Pro986) and has cis/trans isomerase (PPIase) activity essential for proper collagen folding. Recent data suggest that prolyl 3-hydroxylation of Pro986 is not required for the structural stability of collagen; however, the absence of this post-translational modification may disrupt protein-protein interactions integral for proper collagen folding and lead to collagen over-modification. P3H1 and CRTAP stabilize each other and absence of one results in degradation of the other. Hence, hypomorphic or loss of function mutations of either gene cause loss of the whole complex and its associated functions. The relative contribution of losing this complex's 3-hydroxylation versus PPIase and collagen chaperone activities to the phenotype of recessive OI is unknown. To distinguish between these functions, we generated knock-in mice carrying a single amino acid substitution in the catalytic site of P3h1 (Lepre1(H662A) ). This substitution abolished P3h1 activity but retained ability to form a complex with Crtap and thus the collagen chaperone function. Knock-in mice showed absence of prolyl 3-hydroxylation at Pro986 of the α1(I) and α1(II) collagen chains but no significant over-modification at other collagen residues. They were normal in appearance, had no growth defects and normal cartilage growth plate histology but showed decreased trabecular bone mass. This new mouse model recapitulates elements of the bone phenotype of OI but not the cartilage and growth phenotypes caused by loss of the prolyl 3-hydroxylation complex. Our observations suggest differential tissue consequences due to selective inactivation of P3H1 hydroxylase activity versus complete ablation of the prolyl 3-hydroxylation complex.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 24465224 · DOI · PMC3900401
Bisphenol A Exposure and Sperm ACHE Hydroxymethylation in Men [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Exposure to bisphenol A (BPA) has been shown to impact human sperm quality.
- Closing excerpt
- In conclusion, 5hmC of the sperm ACHE gene was positively associated with BPA exposure, which may provide supportive evidence for BPA's effects on male fertility or other health endpoints.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (240 words)
Exposure to bisphenol A (BPA) has been shown to impact human sperm quality. The epigenetic mechanisms underlying the effect remain unknown. The acetylcholinesterase (ACHE) gene is a sperm-expressed gene encoding the acetylcholine hydrolyzing enzyme acetylcholinesterase and participates in the apoptosis of cells, including sperm. This study aimed to examine whether BPA exposure is associated with the hydroxymethylation level of the sperm ACHE gene. A total of 157 male factory workers were studied, among whom 74 had BPA exposure in the workplace (BPA exposure group) and 83 had no BPA exposure in the workplace (control group). Urine samples were collected for BPA measurement and semen samples were collected to assay for ACHE hydroxymethylation. Sperm ACHE hydroxymethylation level was higher in the BPA exposure group (p = 0.041) compared to the control group. When subjects were categorized according to tertiles of detected BPA level, higher ACHE hydroxymethylation levels were observed for the lowest, middle, and top tertiles compared to those with BPA below the limit of detection (LOD). In a linear regression analysis adjusted for confounders, a positive linear association between urine BPA concentration and 5-hydroxymethylcytosine (5hmC) rate of the sperm ACHE gene was observed, although the association did not reach statistical significance in all categories after being stratified by the BPA tertile. In conclusion, 5hmC of the sperm ACHE gene was positively associated with BPA exposure, which may provide supportive evidence for BPA's effects on male fertility or other health endpoints.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30626059 · DOI · PMC6339044
Hypoxia reduces the efficiency of elisidepsin by inhibiting hydroxylation and altering the structure of lipid rafts [3]
Abstract reading summary — source excerpts
- Opening excerpt
- The mechanism of action of elisidepsin (PM02734, Irvalec®) is assumed to involve membrane permeabilization via attacking lipid rafts and hydroxylated lipids.
- Closing excerpt
- Testing for tumor hypoxia or the density of hydroxylated lipids could be an interesting strategy to increase the efficiency of elisidepsin.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (199 words)
The mechanism of action of elisidepsin (PM02734, Irvalec®) is assumed to involve membrane permeabilization via attacking lipid rafts and hydroxylated lipids. Here we investigate the role of hypoxia in the mechanism of action of elisidepsin. Culturing under hypoxic conditions increased the half-maximal inhibitory concentration and decreased the drug's binding to almost all cell lines which was reversed by incubation of cells with 2-hydroxy palmitic acid. The expression of fatty acid 2-hydroxylase was strongly correlated with the efficiency of the drug and inversely correlated with the effect of hypoxia. Number and brightness analysis and fluorescence anisotropy experiments showed that hypoxia decreased the clustering of lipid rafts and altered the structure of the plasma membrane. Although the binding of elisidepsin to the membrane is non-cooperative, its membrane permeabilizing effect is characterized by a Hill coefficient of ~3.3. The latter finding is in agreement with elisidepsin-induced clusters of lipid raft-anchored GFP visualized by confocal microscopy. We propose that the concentration of elisidepsin needs to reach a critical level in the membrane above which elisidepsin induces the disruption of the cell membrane. Testing for tumor hypoxia or the density of hydroxylated lipids could be an interesting strategy to increase the efficiency of elisidepsin.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 24317474 · DOI · PMC3877891
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Using proteins in their natural environment: potential and limitations of microbial whole-cell hydroxylations in applied biocatalysis [4]
- Research article Hyperhydroxylation: a new strategy for neuronal targeting by venomous marine molluscs [5]
- Research article Hydroxylation mediates chromatin demethylation [6]
- Research article Alkane biohydroxylation: Interests, constraints and future developments [7]
- Research article Evaluation of drug-metabolizing enzyme hydroxylation phenotypes in Hispanic populations: the CEIBA cocktail [8]
- Research article [Advances in hydroxylation of hydrophobic amino acid] [9]
References
- Homan EP, Lietman C, Grafe I, Lennington J, Morello R, Napierala D, et al.. Differential effects of collagen prolyl 3-hydroxylation on skeletal tissues. . 2014. PMID 24465224 · DOI · PMC3900401
- Song X, Miao M, Zhou X, Li D, Tian Y, Liang H, et al.. Bisphenol A Exposure and Sperm ACHE Hydroxymethylation in Men. . 2019. PMID 30626059 · DOI · PMC6339044
- Király A, Váradi T, Hajdu T, Rühl R, Galmarini CM, Szöllősi J, et al.. Hypoxia reduces the efficiency of elisidepsin by inhibiting hydroxylation and altering the structure of lipid rafts. . 2013. PMID 24317474 · DOI · PMC3877891
- Duetz WA, van Beilen JB, Witholt B. Using proteins in their natural environment: potential and limitations of microbial whole-cell hydroxylations in applied biocatalysis. Curr Opin Biotechnol. 2001. PMID 11551473 · DOI
- Franco A, Pisarewicz K, Moller C, Mora D, Fields GB, Marì F. Hyperhydroxylation: a new strategy for neuronal targeting by venomous marine molluscs. Prog Mol Subcell Biol. 2006. PMID 17153339 · DOI
- Tsukada Y. Hydroxylation mediates chromatin demethylation. J Biochem. 2012. PMID 22247561 · DOI
- Soussan L, Pen N, Belleville MP, Marcano JS, Paolucci-Jeanjean D. Alkane biohydroxylation: Interests, constraints and future developments. J Biotechnol. 2016. PMID 26853477 · DOI
- de Andrés F, Sosa-Macías M, Lazalde-Ramos BP, Naranjo ME, Tarazona-Santos E, Llerena A, et al.. Evaluation of drug-metabolizing enzyme hydroxylation phenotypes in Hispanic populations: the CEIBA cocktail. Drug Metabol Drug Interact. 2013. PMID 23787463 · DOI
- Sun D, Cheng X, Guo Q, Xu P, Zhu Z, Qin H, et al.. [Advances in hydroxylation of hydrophobic amino acid]. Sheng Wu Gong Cheng Xue Bao. 2018. PMID 30058304 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.