Erucic acid

Erucic Acid: A Comprehensive Encyclopedic Reference

1. Identity and Chemical Characterization

Names and Nomenclature

Erucic acid is a monounsaturated omega-9 fatty acid, denoted 22:1ω9. It is also known as cis-13-docosenoic acid, and its trans isomer is known as brassidic acid. The name derives from the Latin word eruca, meaning arugula or garden rocket (Eruca sativa, a flowering plant of the family Brassicaceae, synonym Cruciferae). It belongs to the group of unsaturated fatty acids (one cis (Z) double bond) in which the double bond from the methyl end is at the omega-9 (ω-9) or n-9 position, so it is written in shorthand as 22:1n-9. It is a member of the subgroup called very long chain fatty acids (VLCFA), defined as those with 20 or more carbon atoms.

Its molecular weight is 338.56768 g/mol; molecular formula C₂₂H₄₂O₂; IUPAC name: (Z)-docos-13-enoic acid; CAS registry number: 112-86-7; PubChem CID: 5281116. Additional synonyms include cis-13-docosenoic acid, 13-cis-docosenoic acid, (Z)-docos-13-enoic acid, 22:1n-9, and delta-13-cis-docosenoic acid.

Physical Properties

Physically, erucic acid appears as a white, waxy solid with a melting point of 33.5–33.8 °C and is soluble in organic solvents like ethanol and ether but insoluble in water. Its boiling point is 381.5 °C (718.7 °F; 654.65 K) at 760 mm Hg.

2. Natural Sources and Botanical Origin

Erucic acid (EA) is a monounsaturated fatty acid (22:1 n-9), synthesized in the seeds of many plants from the Brassicaceae family, with Brassica napus, B. rapa, or B. carinata considered its richest sources. Some species and related varieties of Brassica napus, B. rapa, or B. carinata contain 40–50% erucic acid of the total seed oil.

Erucic acid occurs as a glycerol ester particularly in the seed fats of several Brassicaceae including rapeseed (Brassica napus), mustard (Brassica juncea and Brassica nigra), up to 40–50 percent of the corresponding seed oils (e.g., rapeseed oil), and also wallflower, kale, Brussels sprout, and broccoli — other members of the Brassicaceae.

A reported content of 20 to 54% is found in high erucic acid rapeseed oil, and 42% in mustard oil. It has also been reported in some marine animal oils. A significant level of erucic acid is reported in the brown alga Dictyota dichotoma.

The compound can also be found in other oils, including sunflower oil (up to 900 mg/100 g), and in popular food products such as cereals (up to 500 mg/100 g), pastries (up to 600 mg/100 g), salmon (up to 800 mg/100 g), and nuts (up to 300 mg/100 g).

The erucic acid content in seeds depends on several factors, including irrigation, temperature, soil fertility, day length, and infection.

Common Preparations and Forms

Erucic acid is found in three principal forms in commerce and research: (1) as a constituent of crude, unrefined high-erucic acid rapeseed oil (HEAR) or mustard oil; (2) as a purified fatty acid isolate or as its triglyceride form, glyceryl trierucate; and (3) as the pharmaceutical preparation known as Lorenzo's oil. Lorenzo's oil is a liquid solution made of 4 parts glycerol trioleate and 1 part glycerol trierucate, which are the triacylglycerol forms of oleic acid and erucic acid. It is prepared from olive oil and rapeseed oil.

For industrial purposes and production of erucic acid, rapeseed is used; for food purposes a 'low-erucic acid rapeseed' (LEAR) has been developed (canola), which contains fats derived from oleic acid instead of erucic acid. This led to the creation of low-erucic acid rapeseed (LEAR) oil, which is widely marketed today under the trade name canola oil. The term "canola" is often cited as an acronym for "Canadian Oil, Low Acid," reflecting its origin and primary characteristic.

3. Historical and Traditional Use

Brassica oilseed varieties are some of the oldest plants cultivated, with documentation of their use tracing back to India from 4,000 years ago, and use in China and Japan 2,000 years ago. Their use in Northern Europe for oil lamps is documented to have started in the 13th century.

Rapeseed oil extracts were first put on the market in 1956–1957 as food products, but these had several unacceptable properties. That form of rapeseed oil had a distinctive taste and a greenish colour due to the presence of chlorophyll, and still contained a higher concentration of erucic acid.

High-erucic acid mustard oil has historically been a staple cooking oil in South Asian cultures. In India, mustard oil is used in cooking. It is most popularly used as a cooking oil or condiment in the cuisines of East and Central Asian countries such as China, Bangladesh, and India, but also appears in some dishes in Russian and other Baltic cuisines.

Traditional medicinal uses of high-erucic acid oils (particularly mustard oil) span multiple cultural traditions. These uses should be understood as pertaining to the parent oils — which contain erucic acid along with many other constituents — rather than to purified erucic acid, which was not identified as a distinct compound until the modern chemical era. Folk remedies in Europe, Asia, and the Middle East highlighted the use of mustard oil in massage therapies to alleviate muscular aches, joint pain, and inflammation, as well as in poultices for respiratory issues. In Ayurvedic practice, mustard oil was praised for its warming properties, believed to stimulate circulation and fortify the immune system.

Chinese rapeseed oil was originally extracted from field mustard. In the 19th century, rapeseed (B. rapa) was introduced by European traders, and local farmers crossed the new plant with field mustard to produce semi-winter rapeseed. The seeds were roasted and expeller-pressed to obtain the oil. The resultant oil is heat-stable and fundamental to Sichuan cuisine.

Important distinction: Traditional uses described above pertain to whole plant oils rich in erucic acid. There is no documented historical tradition of using isolated erucic acid as a therapeutic agent. The deliberate therapeutic use of erucic acid as a defined chemical compound began with the development of Lorenzo's oil in the 1980s.

4. Key Constituents, Biosynthesis, and Mechanisms of Action

Biosynthesis

Erucic acid is produced by elongation of oleic acid via oleoyl-coenzyme A and malonyl-CoA. It is an elongation product of oleic acid, and in animals, dietary erucic acid can be retroconverted to oleic acid. Erucic acid is broken down into shorter-chain fatty acids in the human liver by the long-chain acyl CoA dehydrogenase enzyme.

Mechanisms of Action — Relevant to Pharmacological Use

Inhibition of Very Long Chain Fatty Acid (VLCFA) Synthesis

In X-ALD, mutations in ABCD1 impair peroxisomal import and degradation of VLCFAs, leading to accumulation — particularly hexacosanoic acid (C26:0) — that disrupts myelin and fuels neuroinflammation. Lorenzo's oil was designed to lower saturated VLCFAs by competing with fatty-acid elongation enzymes, thereby reducing endogenous production of C24:0 and C26:0. The erucic component appears especially important for inhibiting ELOVL1-mediated elongation — the pathway that generates saturated VLCFAs.

PPAR-δ Agonism

The transcription factor PPARδ is involved in suppressing inflammation, stimulating oligodendroglial biogenesis and myelination, protecting mitochondria against noxious stimuli, and stimulating biogenesis of new mitochondria. PPARδ activation directly inhibits neuronal cell death and reduces both the level and neurotoxicity of Amyloid-β fibers in Alzheimer's Disease models. Among the important ligands of PPARδ is erucic acid (EA, 22:1 n9), an edible omega-9 fatty acid and a component of Lorenzo's oil.

Conversion to Nervonic Acid

EA can also be converted to nervonic acid, an important component of myelin. Hence, EA may act as an anti-inflammatory and remyelinating agent, which might be important in the management of demyelinating diseases.

Anti-inflammatory and Antioxidant Effects

EA exerts antioxidant and anti-inflammatory effects and is a ligand of PPAR-δ. Erucic acid exerts antioxidative and anti-inflammatory efficacies, including inhibition of thrombin and elastase.

Cardiac Mitochondrial Metabolism

The cause of cardiac lipidosis in animals appears to be poor mitochondrial beta-oxidation of this fatty acid, especially in the heart, resulting in an accumulation of erucic acid in neutral lipid droplets. There is primarily an increase in triacylglycerol, while the levels of phospholipids and cholesterol remain relatively constant.

5. Scientific Evidence by Area of Use

5.1 X-Linked Adrenoleukodystrophy (X-ALD) — Lorenzo's Oil

This is the most extensively studied clinical application of erucic acid. Lorenzo's oil is a combination of erucic acid and oleic acid. It is named after Lorenzo Odone, who had adrenoleukodystrophy (ALD). Two rare genetic disorders, ALD and adrenomyeloneuropathy (AMN), can cause a large build-up of certain chemicals called very long-chain fatty acids. The build-up of these fatty acids is thought to cause serious problems in the brain and body. Lorenzo's oil might help prevent some of this build-up.

Biochemical Efficacy

Certain monounsaturated long chain fatty acids including oleic and erucic acids, known as Lorenzo's oil, lower plasma C26:0 levels. This biochemical effect is well-established. By week 10 of treatment, plasma very-long-chain fatty acid levels declined nearly to normal in a two-year open trial of patients with adrenomyeloneuropathy.

Evidence in Symptomatic Patients (AMN)

In a key open trial, 14 men with adrenomyeloneuropathy, 5 symptomatic heterozygous women, and 5 boys (mean age 13 years) with preclinical adrenomyeloneuropathy received a low-fat diet with daily doses of glycerol trioleate oil (1.7 g per kilogram of body weight) and glycerol trierucate oil (0.3 g per kilogram). Over a mean follow-up of 33 months, none of the 14 men with adrenomyeloneuropathy improved. In nine men there was functional deterioration, coincident in four with new cerebral lesions on MRI. In this open trial there was no evidence of a clinically relevant benefit from dietary treatment with oleic and erucic acids in patients with adrenomyeloneuropathy.

While Lorenzo's oil lowered levels of C26:0 in plasma and adipose tissue, it failed to alter levels of C26:0 in the brain. The authors concluded: "failure of erucic acid to enter the brain in significant quantity may be a factor in the disappointing results of dietary therapy for ALD." Another study provided experimental evidence that erucic acid does enter the brain but is rapidly metabolized.

Evidence strength: No clinical benefit demonstrated in symptomatic patients with AMN (one open-label trial, N=24 adults; no randomized controlled trials).

Evidence in Asymptomatic Boys with X-ALD

A single-arm study identified asymptomatic boys with X-linked adrenoleukodystrophy who had a normal MRI. Eighty-nine boys (mean baseline age 4.7 ± 4.1 years; range 0.2–15 years) were identified by a plasma very long-chain fatty acids assay used to screen at-risk boys. All were treated with Lorenzo's oil and moderate fat restriction. Plasma fatty acids and clinical status were followed for 6.9 ± 2.7 years. Of the 89 boys, 24% developed MRI abnormalities and 11% developed both neurological and MRI abnormalities. Abnormalities occurred only in the 64 patients who were aged 7 years or younger at the time therapy was started. There was a significant association between the development of MRI abnormalities and a plasma hexacosanoic acid increase. In this single-arm study, hexacosanoic acid reduction by Lorenzo's oil was associated with reduced risk of developing MRI abnormalities. The authors recommended Lorenzo's oil therapy in asymptomatic boys with X-linked adrenoleukodystrophy who have normal brain MRI results.

A population pharmacodynamic modelling study was performed on 2,384 samples collected during an open label single arm trial. The subjects (n = 104) were administered LO daily at approximately 2–3 mg kg⁻¹ with a mean follow-up of 4.88 ± 2.76 years.

Evidence strength: Single-arm, uncontrolled studies showing a biochemical benefit (VLCFA reduction) and an association with reduced MRI progression in asymptomatic children. No randomized controlled trial exists, partly because of ethical constraints given the rarity of the disease. In the US, Lorenzo's oil is available only to patients participating in a clinical trial.

Lorenzo's oil lowers plasma VLCFA levels within weeks when paired with dietary fat restriction; in long-term follow-up of asymptomatic boys with normal MRI, sustained biochemical control correlated with lower risk of evolving to cerebral disease. The oil does not repair established demyelination, reverse neurologic disability, or halt rapidly progressive cerebral ALD once MRI lesions are active.

5.2 Neurodegenerative Diseases — PPAR-δ Pathway

Research into erucic acid's role in neurodegeneration via its PPAR-δ agonist activity is currently at the preclinical and review-article stage. No human clinical trials of isolated erucic acid for these conditions have been published.

PPARδ activation directly inhibits neuronal cell death and reduces both the level and neurotoxicity of Amyloid-β fibers in Alzheimer's Disease models. Among the important ligands of PPARδ is erucic acid (EA, 22:1 n9), an edible omega-9 fatty acid. Nonetheless, the feature of PPARδ-erucic acid interaction has not been extensively studied.

Increasing evidence suggests a key role of oligodendroglial injury and demyelination in the pathophysiology of Huntington's Disease (HD) and the transcription factor PPARδ is critical for oligodendroglial regeneration and myelination. PPARδ directly involves in the pathogenesis of HD and treatment with a brain-permeable PPARδ-agonist (KD3010) alleviates severity in mice. Erucic acid (EA) is also a PPARδ-ligand ω9 fatty acid which is highly consumed in Asian countries.

Evidence strength: Preclinical only (in vitro cell models and animal studies). No human clinical trials have been conducted for EA in Alzheimer's disease, multiple sclerosis, or Huntington's disease.

5.3 Anticancer Research

Research into erucic acid's anticancer effects is at an early, largely preclinical stage.

A few studies have investigated the cytotoxic potential of EA. No impact on the viability of three human breast cancer cell lines (malignant MCF-7 and MDA-MB-231, and non-malignant HBL-100) was observed at concentrations of EA up to 100 µM. In other studies, EA inhibited the colony formation of human glioma C6 cells and CRL11372 osteoblasts in soft agar in vitro. For both cell lines, the concentration of 100 µM was most effective, with 53 and 25.18% inhibition respectively, when compared to the control.

The anticancer effect was also tested in vivo by the administration of low doses (5 mg daily, i.p., corresponding to 250 mg/kg) of EA to mice (n = 16) with Ehrlich tumor, which extended the survival of the animals to 27 days, in comparison to 20.75 days in the control, untreated group.

One study demonstrated that EA inhibited soft agar colony formation and DNA-synthesis in 3D-spheroids of C6 glioma at therapeutically achievable concentrations. Antitumor effects of EA were more prominent in 3D-growth tests.

ErA exhibited antitumor effects by causing apoptosis and oxidative stress in tumor cells. The apoptotic and Ca²⁺ signaling pathways in tumor cells are triggered when mitochondrial Ca²⁺ and Zn²⁺ accumulation produces reactive free oxygen species (ROS), which in turn activate TRPM2. ErA-induced ROS and TRPM2 stimulation may augment the anticancer action of cisplatin. The cells were divided into groups: control, ErA (200 µM for 48 h), cisplatin (25 µM for 24 h), and ErA + cisplatin + TRPM2 antagonists.

Results in a prostate cancer cell line showed an almost two-fold increase in the cytotoxic activity of the combination of ciprofloxacin and moxifloxacin with erucic acid when compared to the compounds alone.

Erucic acid, an omega-9 monounsaturated fatty acid present in Brassicaceae plants, is highly consumed by the Chinese population. Erucic acid is an activating ligand of the transcription factor PPARδ and an inhibitor of the transcriptional activity of PPARγ, which drive tumorigenesis of glioblastomas and medulloblastomas.

Evidence strength: Preclinical only — in vitro cell lines and mouse models. No human clinical trials have been conducted for erucic acid as an anticancer agent.

6. Body Systems and Health Areas Associated with Erucic Acid

• Nervous system / Peroxisomal metabolism: Central to the clinical application in X-ALD via VLCFA pathway inhibition.
• Cardiovascular system: Unlike some other monounsaturated fatty acids which may reduce the risk of heart disease, experimental animal studies have shown that exposure to diets with oils containing excessive erucic acid may lead to adverse health effects, with the heart as the principal target organ. The most common effect in experimental animals is myocardial lipidosis, an accumulation of lipids in heart muscle fibres that may reduce the contractile force of heart muscles.
• Myelin sheath integrity: EA is an ingredient of Lorenzo's oil employed in the medical treatment of adrenoleukodystrophy and can be converted to nervonic acid, a component of myelin.
• Neurological / anti-inflammatory: Via PPAR-δ agonism, EA has demonstrated anti-neuroinflammatory properties in preclinical models.
• Hematological: Erucic acid at therapeutic doses used in Lorenzo's oil protocols affects platelet count and function (see Safety section).
• Hepatic: Previous studies have reported that EA consumption caused myocardial lipidosis and hepatic steatosis.

7. Dosage Forms and Dosages Reported in Studies

The following dosages are stated as reported in the cited sources and pertain specifically to therapeutic or investigational contexts, not to dietary intake from food.

• Lorenzo's oil (ALD treatment protocol — Aubourg et al., NEJM 1993): 14 men with adrenomyeloneuropathy, 5 symptomatic heterozygous women, and 5 boys received daily doses of glycerol trioleate oil (1.7 g per kilogram of body weight) and glycerol trierucate oil (0.3 g per kilogram of body weight), on a low-fat diet.
• Lorenzo's oil (Moser et al. follow-up study, 2005): One protocol contained 20 percent erucic acid (22:1) and 80 percent oleic acid (18:1). 40 male and 6 female patients received Lorenzo's Oil according to a protocol calculated to provide 20 percent of daily caloric intake.
• Lorenzo's oil (Ahmed et al. PK/PD model, 2016): 2,384 samples were analysed from an open label single arm trial. Subjects (n = 104) were administered LO daily at approximately 2–3 mg kg⁻¹ with a mean follow-up of 4.88 ± 2.76 years.
• Anticancer (in vivo mouse, Ehrlich tumor model): Administration of low doses (5 mg daily, i.p., corresponding to 250 mg/kg) of EA to mice (n = 16) with Ehrlich tumor.
• In vitro anticancer (HT-29 colorectal cancer cells): Cells were treated with ErA (200 µM for 48 h), cisplatin (25 µM for 24 h), and ErA + cisplatin + TRPM2 antagonists.
• In vitro glioma (colony formation assay): EA inhibited the colony formation of human glioma C6 cells and CRL11372 osteoblasts in soft agar in vitro. For both cell lines, the concentration of 100 µM was most effective.

8. Regulatory Limits on Dietary Exposure

The European Food Safety Authority (EFSA) published a risk assessment of erucic acid in feed and food in 2016, establishing a Tolerable Daily Intake (TDI) for humans of 7 mg/kg body weight per day based on the occurrence of cardiac lipidosis in experimental animals.

By applying an uncertainty factor of 100 (10 for extrapolation from experimental animals to humans, 10 for variation within humans), a tolerable level for human exposure of 7.5 mg erucic acid/kg body weight per day (approximately 500 mg erucic acid/day for an average adult) was derived.

A tolerable daily intake (TDI) of 7 mg/kg body weight per day for erucic acid was established, based on a no observed adverse effect level (NOAEL) of 0.7 g/kg bw per day for lipidosis in young rats. Myocardial lipidosis, as reported in rats and pigs following feeding with HEAR oils, was selected as the critical effect. Since there are no adequate data from human studies for dose–response assessment, the CONTAM Panel considered data from studies on experimental animals. The CONTAM Panel selected the overall NOAEL for lipidosis of 0.7 g/kg bw per day, observed in a 7-day feeding study in young rats and in a 2-week feeding study in newborn piglets, as the reference point.

The mean chronic exposure of the different population groups does not exceed the TDI and is between 0.3 mg/kg and 4.4 mg/kg body weight per day. However, the level of dietary exposure was higher in infants and children, ranging from 1.3 to 7.4 mg/kg body weight per day, which is a risk for young people with high exposure to erucic acid, since the highest level of this range coincides with the value of the TDI.

For most humans, the main contributor to dietary exposure to erucic acid is the food group 'fine bakery wares'. In infants, 'food for infants and small children' is the main contributor to exposure.

Food-grade rapeseed oil (also known as canola oil, rapeseed 00 oil, low erucic acid rapeseed oil, LEAR oil) is regulated to a maximum of 2% erucic acid by weight in the US and Europe.

In 2003, Food Standards Australia set a provisional tolerable daily intake (PTDI) for an average adult of approximately 500 mg/day of erucic acid, extrapolated based on the level associated with increased myocardial lipidosis in nursing pigs.

Erucic acid content increases with total fat content, both in farmed and wild fish, and it is particularly high in fish liver, fish oil, and oily fish such as mackerel. The current TDI could be exceeded with a 200 g meal of mackerel, as at the maximum concentration analyzed, such a meal would contribute 143% to the TDI.

The regulations on mustard oil began in 1976 when the EU introduced a maximum level of 5% erucic acid contribution to the total fatty acids in edible oils. The US followed suit in the 1990s when the FDA banned the import and sale of mustard oil as foodstuffs.

9. Safety Considerations

9.1 Cardiac Toxicity in Animal Models

The heart is the principal target organ for toxic effects after erucic acid exposure. Myocardial lipidosis was identified as the critical effect for chronic exposure. This effect is reversible and transient during prolonged exposure.

It had been demonstrated that the long-chain monounsaturated erucic acid accumulates due to inhibition of β-oxidation in the mitochondria. However, after 4 to 6 weeks the lipid accumulation decreased and disappeared after 4 weeks. After long-term feeding with pure erucic acid alone, unlike what was seen with diverse rapeseed oil types, no increase of focal necrosis and fibrosis in the epicardial region of the myocardium was observed. The microscopic picture of myocardium was similar to those seen for sunflower seed oil used in the control group. This supported the conclusion that erucic acid was not the only factor responsible for long-term adverse lesions.

9.2 Human Cardiac Evidence — Absence of Confirmed Harm

As the compound was blamed for the poisoning effect in Toxic Oil Syndrome, and some data indicated its cardiotoxicity to rats, EA was for decades classified as a toxic substance. However, the cardiac adverse effects of EA have not been confirmed in humans, and the experiments in animal models had many limitations.

The adverse cardiac effect has not been proven in human subjects, whereas in rats it is reversible.

Severe cardiomyopathy was observed among consumers of rapeseed oils rich in EA in the Spanish Toxic Oil Syndrome. It was proposed that EA is highly toxic to cardiac mitochondria. However, several studies showed that those cases were seen only among consumers of rapeseed oils which were refined with carcinogenic aniline dyes.

There are no reports of toxicity from dietary consumption of erucic acid.

9.3 Hematological Effects at Therapeutic Doses (Lorenzo's Oil)

In a clinical trial for the management of adrenoleukodystrophy, researchers analyzed the effect of erucic acid (a component of Lorenzo's oil) on platelet number, fatty acid composition, and function. Platelet levels of erucic acid were markedly elevated, whereas those of linoleic and arachidonic acid were reduced. In six patients with thrombocytopenia, there was an inverse correlation between the number of platelets and the percentage of erucic acid in platelets. In 6 patients with thrombocytopenia, platelet counts became normal within 2 to 3 months after erucic acid was omitted from the diet.

The oil has been shown to cause a lowered platelet count, which can lead to thrombocytopenia and lymphopenia. Low platelet count and bleeding diathesis have been observed in patients with adrenoleukodystrophy treated with erucic acid (22:1)-rich triglycerides ('Lorenzo's oil').

9.4 Brain Penetration Limitation

While Lorenzo's oil lowered levels of C26:0 in plasma and adipose tissue, it failed to alter levels of C26:0 in the brain. The authors concluded that failure of erucic acid to enter the brain in significant quantity may be a factor in the disappointing results of dietary therapy for ALD. This may be explained by another study that provided experimental evidence that erucic acid does enter the brain but is rapidly metabolized.

9.5 Hepatic Effects

Erucic acid has demonstrated effects including ameliorating myocardial lipidosis, congestive heart disease, hepatic steatosis, and memory impairments in rodent models. These findings prompted regulatory bodies to establish limits on EA content in food oils. The studies were performed on rodents and led to caution on ingesting EA at high levels.

9.6 Regulatory Access Status

In the US, Lorenzo's oil is only available to patients participating in a clinical trial. Mustard oil containing 20–40% EA was banned for consumption by the US FDA.

References

• Galanty A, et al. "Erucic Acid—Both Sides of the Story: A Concise Review on Its Beneficial and Toxic Properties." Molecules. 2023 Feb 17;28(4):1924. PMC9962393.
• EFSA CONTAM Panel. "Erucic acid in feed and food." EFSA Journal. 2016;14(11):4593.
• EFSA CONTAM Panel. "Erucic acid in feed and food." Wiley/EFSA Journal. 2016.
• Aubourg P, et al. "A two-year trial of oleic and erucic acids ('Lorenzo's oil') as treatment for adrenomyeloneuropathy." N Engl J Med. 1993;329(11):745-52. PMID: 8350883.
• Moser HW, et al. "Follow-up of 89 asymptomatic patients with adrenoleukodystrophy treated with Lorenzo's oil." Arch Neurol. 2005;62(7):1073-80. PMID: 16009761.
• Ahmed MA, et al. "A model-based approach to assess the exposure-response relationship of Lorenzo's oil in adrenoleukodystrophy." Br J Clin Pharmacol. 2016;81(6):1058-66. PMC4876192.
• Altinoz MA, Ozpinar A. "PPAR-δ and erucic acid in multiple sclerosis and Alzheimer's Disease. Likely benefits in terms of immunity and metabolism." Int Immunopharmacol. 2019;69:245-256. PMID: 30738994.
• Altinoz MA, et al. "Erucic acid, a nutritional PPARδ-ligand may influence Huntington's disease pathogenesis." Metab Brain Dis. 2019. Springer Nature.
• Altinoz MA. "Could dietary erucic acid lower risk of brain tumors? An epidemiological look to Chinese population." Metab Brain Dis. 2022 Dec;37(8):2643-2651. PMID: 35704146.
• Nazıroğlu M, et al. "Erucic acid increases the potency of cisplatin-induced colorectal cancer cell death and oxidative stress by upregulating the TRPM2 channel." Cell Biology International. 2024.
• Altinoz MA, Bilir A, Elmaci I. "Erucic acid, a component of Lorenzo's oil and PPAR-δ ligand modifies C6 glioma growth and toxicity of doxorubicin." Chem Biol Interact. 2018;294:107-117.
• Sanden M, et al. "Erucic Acid (22:1n-9) in Fish Feed, Farmed, and Wild Fish and Seafood Products." PMC6212994.
• Kickler TS, Zinkham WH, Moser A, et al. "Effect of erucic acid on platelets in patients with adrenoleukodystrophy." Biochem Mol Med. 1996;57:125-33. PMID: 8733890.
• Zinkham WH, Kickler T, Borel J, Moser HW. "Lorenzo's Oil and Thrombocytopenia in Patients with Adrenoleukodystrophy." N Engl J Med. 1993;328(15):1126-7.
• Wikipedia. "Erucic acid." (Accessed 2026).
• ScienceDirect Topics. "Erucic Acid — an overview."
• Centre for Food Safety, Hong Kong. "Erucic Acid in Edible Fats and Oils."
• Food Standards Agency (UK). "Rapid Risk Assessment: Long-term risk of erucic acid to UK consumers."
• PubChem. "Erucic Acid | C22H42O2 | CID 5281116."
• Kumar JBS, Sharma B. "Review of the potential pharmacological role of erucic acid: a monounsaturated omega-9 fatty acid." Naunyn-Schmiedeberg's Arch Pharmacol. 2023.