Malonaldehyde

72 °C

72 °C

161 °F

Solid (needles); [NIOSH]

Solid

NEEDLES.

Solid (needles).

Evidence of injury to the liver and pancreas in mice experiments when added to drinking water at 500 mg/kg body weight per day; [HSDB] No listed effects of short-term or long-term exposure; [ICSC] May cause skin, eye, and respiratory tract irritation; Excessive exposure may cause CNS depression; [Merck Index] Causes muscle weakness, dyspnea, and cyanosis in oral lethal-dose study of rats; Causes other gastrointestinal and liver changes and inflammation, necrosis, or scarring of bladder in 90-day oral study of mice; [RTECS] See ALDEHYDES

DHHS/NTP; Toxicology & Carcinogenesis Studies of Malonaldehyde, Sodium Salt (3-Hydroxy-2-propenal, sodium salt) in F344/N Rats and B6C3F1 Mice (Gavage Studies) Technical Report Series No. 331 (1988) NIH Publication No. 88-1792 /Malonaldehyde, sodium salt/

NIOSH considers maloaldehyde to be a potential occupational carcinogen.

NIOSH usually recommends that occupational exposures to carcinogens be limited to the lowest feasible concn.

Proteins [Note: Pure compound is stable under neutral conditions, but not under acidic conditions].

Proteins [Note: Pure compound is stable under neutral conditions, but not under acidic conditions.]

THIOBARBITURIC ACID-REACTING MATERIAL PRODUCED DURING ENZYMIC MICROSOMAL LIPID PEROXIDATION WAS IDENTIFIED AS MALONALDEHYDE. PHOSPHOLIPID ARACHIDONATE WAS ESTABLISHED AS THE MAJOR SOURCE OF THE MALONALDEHYDE PRODUCED IN THE REACTION.

(14)C-ACETATE APPEARED TO BE THE MAJOR ACCUMULATING METABOLITE IN RAT LIVER MITOCHONDRIAL PREPARATIONS FOLLOWING A 120-MINUTE INCUBATION WITH (14)C-MALONALDEHYDE. A PROBABLE BIOCHEMICAL ROUTE FOR MALONALDEHYDE METABOLISM INVOLVES OXIDATION OF MALONALDEHYDE BY MITOCHONDRIAL ALDEHYDE DEHYDROGENASE FOLLOWED BY DECARBOXYLATION TO PRODUCE CARBON DIOXIDE AND ACETATE.

Two aldehyde dehydrogenases in the rat-liver cytosol fraction account for virtually all of the metabolizing activity for malonaldehyde.

After oral administration of malonaldehyde (158 mg/kg body weight) to rats, increased quantities of formaldehyde, acetaldehyde, acetone and malonaldehyde itself were found in the urine. Additionally, methyl ethyl ketone, not found in control rats, was present in the urine of the animals that had received malonaldehyde.

Uremic 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.

IN PRIMARY RAT SKIN FIBROBLAST CULTURES GROWN IN A MEDIUM CONTAINING 1X10(-5), 1X10(-4), OR 1X10(-3) MOLAR OF 1,3-(14)C MALONALDEHYDE, THERE WAS A LIMITED, CONCENTRATION-DEPENDENT UPTAKE OF MALONALDEHYDE BY 24 HR (APPROXIMATELY 4% AT ALL CONCENTRATIONS). 83-89% OF THE (14)C WAS OXIDIZED TO (14)CO2 BY 24 HR AND APPROXIMATELY 5% WAS RECOVERED IN THE MAJOR LIPIDS. LIMITED CELLULAR UPTAKE OF MALONALDEHYDE MAY EXPLAIN THE TOLERANCE OF CELLS GROWN IN CULTURE TO RELATIVELY HIGH CONCENTRATIONS.

TWELVE HOURS AFTER INTUBATION WITH 1,3-(14)C MALONALDEHYDE, MALE WISTAR RATS SHOWED 60-70%, 5-15% AND 9-17% OF ADMINISTERED RADIOACTIVITY IN EXPIRED CARBON DIOXIDE, FECES AND URINE, RESPECTIVELY. IN VITRO EXPERIMENTS SHOWED METABOLISM TO BE PRIMARILY IN MITOCHONDRIA VIA REACTIONS INVOLVING OXYGEN UTILIZATION AND (14)CO2 PRODUCTION. THE APPARENT KM AND VMAX WERE 0.5 MMOL AND 9.3 NMOL/MIN/MG PROTEIN FOR OXYGEN UPTAKE, RESPECTIVELY, AND 2.0 MMOL AND 2.4 NMOL/MIN/MG PROTEIN FOR (14)CO2 PRODUCTION.