Malonic Acid

Fires involving this material can be controlled with a dry chemical, carbon dioxide or Halon extinguisher. A water spray may also be used. (NTP, 1992)

Use water spray, powder, foam, carbon dioxide.

Fresh air, rest. Refer for medical attention.

Remove contaminated clothes. Rinse skin with plenty of water or shower.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Rinse mouth. Refer for medical attention .

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

ACCIDENTAL RELEASE MEASURES; Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Do not let product enter drains. Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal.

SMALL SPILLS AND LEAKAGE: If you spill this chemical, you should dampen the solid spill material with water, then transfer the dampened material to a suitable container. Use absorbent paper dampened with water to pick up any remaining material. Seal your contaminated clothing and the absorbent paper in a vapor-tight plastic bag for eventual disposal. Wash all contaminated surfaces with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

SRP: Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.

Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Contaminated packaging: Dispose of as unused product.

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.

Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Further processing of solid materials may result in the formation of combustible dusts. The potential for combustible dust formation should be taken into consideration before additional processing occurs. Provide appropriate exhaust ventilation at places where dust is formed.

ACCIDENTAL RELEASE MEASURES; Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Do not let product enter drains.

Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday.

For more Preventive Measures (Complete) data for Malonic acid (6 total), please visit the HSDB record page.

The present experiments were carried out to provide direct in vivo evidence for the involvement of c-Jun N-terminal kinase (JNK) in the induction of ischemic brain injury. Malonate, which produces lesions similar to those of focal ischemia-reperfusion by a reversible inhibition of succinate dehydrogenase in mitochondria, was injected into the left striatum in the rat brain without or with the simultaneous injection of a cell permeable peptidic JNK inhibitor, (L)-HIV-TAT48-57-PP-JBD20. Two regions of malonate-induced brain injury were visualized as a hyperintense region with surrounding hypointense regions by apparent diffusion coefficient mapping magnetic resonance imaging. The JNK inhibitor significantly counteracted both hyper- and hypointense regions at the early stage of brain injury. Histological examination clarified that the inhibitor suppressed the induction of coagulation necrosis and spongy degeneration at early and late stages. /Malonate/

The acute and long-term effects of the local perfusion of 3,4-methylenedioxymethamphetamine (MDMA) and the interaction with the mitochondrial inhibitor malonate (MAL) were examined in the rat striatum. MDMA, MAL or the combination of MAL with MDMA was reverse dialyzed into the striatum for 8 h via a microdialysis probe while extracellular dopamine (DA) and serotonin (5-HT) were measured. One week later, tissue immediately surrounding the probe was assayed for DA and 5-HT tissue content. Local perfusion of MDMA increased DA and 5-HT release but did not produce long-term depletion of DA or 5-HT in tissue. Malonate also increased both DA and 5-HT release but, in contrast to MDMA, produced only long-term depletion of DA. The combined perfusion of MDMA/MAL synergistically increased the release of DA and 5-HT and produced long-term depletion of both DA and 5-HT in tissue. These results support the conclusion that DA, compared with 5-HT, neurons are more susceptible to mitochondrial inhibition. Moreover, MDMA, which does not normally produce DA depletion in the rat, exacerbated MAL-induced DA depletions. The effect of MDMA in combination with MAL to produce 5-HT depletion suggests a role for bio-energetic stress in MDMA-induced toxicity to 5-HT neurons. Overall, these results highlight the importance of energy balance to the function of DA and 5-HT neurons and to the toxic effects of MDMA. /Malonate/

We examined whether creatine administration could exert neuroprotective effects against excitotoxicity mediated by N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainic acid. Oral administration of 1% creatine significantly attenuated striatal excitotoxic lesions produced by NMDA, but had no effect on lesions produced by AMPA or kainic acid. Both creatine and nicotinamide can exert significant protective effects against malonate-induced striatal lesions. We, therefore, examined whether nicotinamide could exert additive neuroprotective effects with creatine against malonate-induced lesions. Nicotinamide with creatine produced significantly better neuroprotection than creatine alone against malonate-induced lesions. Creatine can, therefore, produce significant neuroprotective effects against NMDA mediated excitotoxic lesions in vivo and the combination of nicotinamide with creatine exerts additive neuroprotective effects. /Malonate/

The mitochondrial inhibitors malonate and 3-nitropropionic (3NP) acid are potent neurotoxins in vivo. Administration of these compounds results in neuronal loss similar to that seen in Huntington's disease. Although the mechanism of cell death produced by these compounds likely involves activation of N-methyl-D-aspartate receptors, it remains unclear why the striatum demonstrates regional susceptibility to the toxicity of these and other mitochondrial poisons. We hypothesized that dopamine, a weak neurotoxin that occurs in high concentrations in the striatum, may contribute to the neuronal damage caused by mitochondrial inhibition. We investigated whether depletion of striatal dopamine using the catecholaminergic toxin 6-hydroxydopamine would attenuate lesions induced by mitochondrial inhibition. We found that dopamine depletion reduced significantly the extent of histological damage in the striatum elicited by both intraparenchymal injections of 0.8 micromol malonate and 20 mg/kg systemic administration of 3NP. These data suggest that dopamine or one of its metabolites may contribute to mitochondrial toxin-induced cell death. /Malonate/

For more Interactions (Complete) data for Malonic acid (7 total), please visit the HSDB record page.

LC50; Species: Daphnia magna (Water Flea) age <24 hr larva, 1st instar; Conditions: freshwater, static, 22 °C, pH 7.7 (7.0-8.2 ug/L); Concentration: 275000 ug/L for 48 hr (95% confidence interval: 233000- 324000 ug/L)

LC50; Species: Lepomis macrochirus (Bluegil); Conditions: freshwater, static, 21-25 °C; Concentration: 150000 ug/L for 24 hr /formulated product/

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 4(SRC), determined from a structure estimation method(2), indicates that malonic acid is expected to have very high mobility in soil(SRC). Respective pKa1 and pKa2 values of 2.8 and 5.7(3), indicate this compound will exist almost entirely in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Volatilization of malonic acid from moist soil surfaces is not expected to be an important fate process(SRC) due to ionization. Based on biodegradation screening results of analogous dicarboxylic acids (succinic acid and oxalic acid), malonic acid is expected to be readily biodegradable(3). In two 5-day BOD studies, malonic acid achieved 38 to 76.6% theoretical BODs(5,6).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 4(SRC), determined from a structure estimation method(2), indicates that malonic acid is not expected to adsorb to suspended solids and sediment(SRC). Respective pKa1 and pKa2 values of 2.8 and 5.7(3), indicate this compound will exist almost entirely in the anion form in the environment and therefore, volatilization from water surfaces is not expected to be an important fate process(SRC). According to a classification scheme(4), an estimated BCF of 3(SRC), from its log Kow of -0.81(5) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Based on biodegradation screening results of analogous dicarboxylic acids (succinic acid and oxalic acid), malonic acid is expected to be readily biodegradable(3). In two 5-day BOD studies, malonic acid achieved 38 to 76.6% theoretical BODs(6,7). Malonic acid is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(8).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), malonic acid, which has a vapor pressure of 2.7X10-6 mm Hg at 23 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase malonic acid is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 10 days(SRC), calculated from its rate constant of 1.6X10-12 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase malonic acid may be removed from the air by wet and dry deposition(SRC). Malonic acid absorbs weakly at wavelengths >290 nm(4) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

Malonic acid has been identified in celery, parsnip, green pepper, tangerine, beet, oats, tabasco, chili, orange, grapefruit, lime, melon, cantaloupe, sunflower, barley, prickly pear, Indian fig, ginseng, black bean, kidney bean, green bean, peach, corn, and banana(1).

Safe in the present practices of use and concentration. Ingredient, concentration, and use information are available in documents discoverable at https://cir-reports.cir-safety.org

IDENTIFICATION AND USE: Malonic acid is used in biochemical and cell studies, as well as in chemical synthesis. This acid is well known as a competitive inhibitor of succinic dehydrogenase, and has been used extensively in investigations of the tricarboxylic acid cycle. It can be used in veterinary medicine to prevent resorption of bone tissue in broiler chicks caused by disturbance of photoperiodism. HUMAN STUDIES: The influence of malonic acid on the proliferation rate of cultured human fetal skin fibroblasts was investigated. Addition of malonate stimulated fibroblast proliferation. The maximum stimulation occurred in the medium at the 0.01 mM concentration of malonic acid. When the cells were cultured in the medium with serum, the influence of malonate on the cells proliferation increased. ANIMAL STUDIES: Malonic acid (MA) is a reversible inhibitor of succinate dehydrogenase (SDH) which induces mitochondrial dysfunction followed by secondary excitotoxicity and apoptosis due to generation of reactive oxygen species. Intrastriatal injection of malonate results in both chemically induced hypoxia and striatal lesions that are similar to those seen in Huntington's disease and cerebral ischemia. Malonic acid was mildly irritating to skin in rats. In an in vitro eye irritation test, malonic acid was considered to be irritating. The behavioral effects of unilateral intrastriatal administration of malonate (0.6, 1.8 or 6 umol) in adult male rats have been reported. Low doses of malonate (1.8 umol) decreased exploratory activity and caused ipsiversive rotational behavior. High doses of malonate (6 umol) induced contralateral rotational behavior and convulsive episodes. Malonate-induced striatal toxicity was significantly reduced following lesions of either the glutamatergic or dopaminergic afferents to the striatum. Intrastriatal injection of malonate produced age-dependent striatal lesions, which were significantly greater in 4- and 12-month-old animals than in 1-month-old animals. Malonic acid was negative for mutagenicity in a bacterial reverse mutation assay.

Cough. Sore throat.

Redness. Pain.

Redness. Pain.

Abdominal pain. Diarrhoea. Nausea. Vomiting.

EPA has released the Interactive Chemical Safety for Sustainability (iCSS) Dashboard. The iCSS Dashboard provides an interactive tool to explore rapid, automated (or in vitro high-throughput) chemical screening data generated by the Toxicity Forecaster (ToxCast) project and the federal Toxicity Testing in the 21st century (Tox21) collaboration. /The title compound was tested by ToxCast and/or Tox21 assays/[USEPA; ICSS Dashboard Application; Available from, as of August 9, 2018: http://actor.epa.gov/dashboard/]

The following link will take the user to the National Toxicology Program (NTP) Test Status of Agents Search page, which tabulates the results and current status of tests such as "Short-Term Toxicity Studies", "Long-term Carcinogenicity Studies", "Developmental Studies", "Genetic Toxicology Studies", etc., performed with this chemical. Testing status for malonic acid is available.[Available from, as of August 9, 2018: https://ntpsearch.niehs.nih.gov/?e=True&ContentType=Testing+Status]

Based on monitoring at a Los Angeles roadway tunnel, the emission rate malonic acid was 14.0 ug/L of gasoline-equivalent burned(1). Malonic acid was detected in effluents from a kraft pulp mill bleach factory(2) and at a concentration of 8.1 mg/L in shale oil process retort water(3).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of malonic acid can be estimated to be 4(SRC). According to a classification scheme(2), this estimated Koc value suggests that malonic acid is expected to have very high mobility in soil. Respective pKa1 and pKa2 values of 2.8 and 5.7(3), indicate this compound will exist almost entirely in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4).