Hexenal

HCID 10460

Notes Reactions

Substructure search Find similar structures

Basic information

CAS: 1335-39-3
Standard SMILES: CCCC=CC=O
InChIKey: MBDOYVRWFFCFHM-UHFFFAOYSA-N
Molecular formula: C6H10O
Average molar mass: 98.14 g/mol
Monoisotopic mass: 98.07316494

Overview

2-Hexenal has been reported in Aethus indicus, Humulus lupulus, and other organisms with data available.

Names & identifiers

Preferred name: Hexenal
IUPAC: hex-2-enal
English name: Hexenal
Molecular formula: C6H10O
Molecular weight: 98.143

Names & synonyms

Hexenal1335-39-3RefChem:787469CHEBI:24578DTXSID1010527182-Hexen-1-alTrans-3-propyalacroleinn-C3H7CH=CHCHO(E)-2-hexen-1-alCHEBI:19591(Z)-2-hexen-1-alEpitope ID:143637

Show more names

SCHEMBL29822SCHEMBL233667DTXSID7021609s6303AKOS025243569SB85391NS00080067D78252

Database identifiers

CAS: 1335-39-3、505-57-7
PubChem CID: 10460
DTXSID: DTXSID7021609

Properties

Computed structural properties

XLogP: 1.5
Topological polar surface area: 17.1 Å²
Hydrogen bond donors: 0
Hydrogen bond acceptors: 1
Rotatable bonds: 3
Heavy atoms: 7
Formal charge: 0
Complexity: 64.6

Experimental & physicochemical properties

SpringerMaterials PropertiesDielectric constant

Physicochemical properties

EPA Substance Registry System: Hexenal (1335-39-3)
TSCA: TSCA listed

Safety & regulation

Hazard information

Regulatory InformationChemical: Hexenal

Other Safety InformationEvaluation - Chemicals not considered for in depth evaluation - Not commercially active in Australia

Toxicology

TreatmentKidney dialysis is usually needed to relieve the symptoms of uremic syndrome until normal kidney function can be restored.

Health EffectsChronic exposure to uremic toxins can lead to a number of conditions including renal damage, chronic kidney disease and cardiovascular disease.

Exposure RoutesEndogenous, Ingestion, Dermal (contact)

Toxicity Summary · 1 item

Uremic toxins such as 2-Hexenal are actively transported into the kidneys via organic ion transporters (especially OAT3). Increased levels of uremic toxins can stimulate the production of reactive oxygen species. This seems to be mediated by the direct binding or inhibition by uremic toxins of the enzyme NADPH oxidase (especially NOX4 which is abundant in the kidneys and heart) (A7868). Reactive oxygen species can induce several different DNA methyltransferases (DNMTs) which are involved in the silencing of a protein known as KLOTHO. KLOTHO has been identified as having important roles in anti-aging, mineral metabolism, and vitamin D metabolism. A number of studies have indicated that KLOTHO mRNA and protein levels are reduced during acute or chronic kidney diseases in response to high local levels of reactive oxygen species (A7869).

Signs and Symptoms · 1 item

As a uremic toxin, this compound can cause uremic syndrome. Uremic syndrome may affect any part of the body and can cause nausea, vomiting, loss of appetite, and weight loss. It can also cause changes in mental status, such as confusion, reduced awareness, agitation, psychosis, seizures, and coma. Abnormal bleeding, such as bleeding spontaneously or profusely from a very minor injury can also occur. Heart problems, such as an irregular heartbeat, inflammation in the sac that surrounds the heart (pericarditis), and increased pressure on the heart can be seen in patients with uremic syndrome. Shortness of breath from fluid buildup in the space between the lungs and the chest wall (pleural effusion) can also be present.

Carcinogen ClassificationNo indication of carcinogenicity to humans (not listed by IARC).

Safety data

tsca: TSCA listed

Chemistry & industry

Pharmacology

Metabolism/MetabolitesUremic toxins tend to accumulate in the blood either through dietary excess or through poor filtration by the kidneys. Most uremic toxins are metabolic waste products and are normally excreted in the urine or feces.

MeSH Pharmacological Classification · 2 items

Drugs used to induce drowsiness or sleep or to reduce psychological excitement or anxiety.

Substances that do not act as agonists or antagonists but do affect the GAMMA-AMINOBUTYRIC ACID receptor-ionophore complex. GABA-A receptors (RECEPTORS, GABA-A) appear to have at least three allosteric sites at which modulators act: a site at which BENZODIAZEPINES act by increasing the opening frequency of GAMMA-AMINOBUTYRIC ACID-activated chloride channels; a site at which BARBITURATES act to prolong the duration of channel opening; and a site at which some steroids may act. GENERAL ANESTHETICS probably act at least partly by potentiating GABAergic responses, but they are not included here.