Even in the absence of other fungal components, oxalic acid, a pathogenicity factor for sclerotinia sclerotiorum, suppresses the host plant's oxidative burst and directly limits the synthesis of H2O2 by soybean cells in response to OGA[1].

Even in the absence of other fungal components, oxalic acid, a pathogenicity factor for sclerotinia sclerotiorum, suppresses the host plant's oxidative burst and directly limits the synthesis of H2O2 by soybean cells in response to OGA[1].

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Oxalic Acid suppressed the oxidative burst (H₂O₂ production) in suspension-cultured tobacco and soybean cells induced by various elicitors, with a median inhibitory concentration (IC₅₀) of approximately 4 to 5 mM. Maximal inhibition was reached at about 6-7 mM. It inhibited bursts induced by oligogalacturonic acid (OGA), a Verticillium elicitor, hypoosmotic shock, cantharidin, and harpin, although the maximal inhibition of the harpin-induced burst was only about 30% of the control. [1]
Filtrate from a wild-type, oxalate-secreting strain of S. sclerotiorum (containing ~12.4 mM oxalate) almost completely suppressed the OGA-induced H₂O₂ production in tobacco cells, whereas filtrate from an oxalate-deficient mutant (containing ~0.11 mM oxalate) did not. Adding 11 mM oxalate to the mutant filtrate restored its inhibitory potency. [1]
The inhibitory effect was largely independent of medium acidification or Ca²⁺ chelation. Oxalate did not inhibit elicitor-stimulated cytosolic Ca²⁺ transients in aequorin-transformed tobacco cells. [1]
Oxalate inhibited the oxidative burst only when added before or during the early phase of elicitor activation; it had no effect once H₂O₂ production had reached its maximal rate, indicating it acts prior to the catalysis by the assembled/activated oxidase complex. [1]

Inoculation of tobacco leaves with an oxalate-deficient, nonpathogenic mutant of S. sclerotiorum induced a measurable oxidative burst (visualized by nitroblue tetrazolium staining), whereas inoculation with a wild-type, oxalate-secreting strain did not. The oxalate-secreting strain successfully colonized the leaf tissue. [1]

H₂O₂ Production Assay: Production of H₂O₂ in plant suspension cell cultures (tobacco or soybean) was monitored fluorometrically by measuring the oxidative quenching of the dye pyranine (excitation 405 nm, emission 512 nm). Cells (1.5 mL) were placed in a fluorometer cuvette with 1 µg/mL pyranine. After addition of an elicitor (e.g., 5 µg/mL OGA), the rate of H₂O₂ biosynthesis was approximated by measuring the maximum rate of fluorescence quenching. Test compounds like Oxalic Acid (pH-adjusted to 5.7) were added at the time of elicitor stimulation or at specified times afterwards. Data are presented as a percentage of the rate for control cells tested on the same day. [1]
Cytosolic Ca²⁺ Measurement: Changes in cytosolic Ca²⁺ concentration were monitored in aequorin-transformed tobacco cells using luminescence measurements. Cells were treated with test compounds (e.g., 10 mM oxalate or 1.5 mM BAPTA-AM) 5 minutes prior to stimulation with an elicitor like OGA. Luminescence was recorded and transformed into corresponding Ca²⁺ concentrations. Residual functional aequorin was quantified after each run by lysing cells with CaCl₂ and detergent. [1]

Absorption, Distribution and Excretion
Tartaric acid and oxalic acid are excreted unchanged in the urine. This study investigated the absorption of 14C-labeled oxalic acid in Wistar rats, CD-1 mice, and NMRI mice. Animals were gavaged with an oxalic acid solution mixed with either water or 0.625 g/kg body weight of xylitol. Animals acclimated to xylitol and those previously unexposed to xylitol were used. Xylitol-acclimated mice showed enhanced absorption and urinary excretion of the label (oxalic acid) in both mouse strains, but this was not observed in rats. Previous studies have shown a higher incidence of bladder stones in mice fed high doses of xylitol, but this was not observed in rats. The results of this study provide a possible explanation for increased bladder stone formation due to urinary oxalate supersaturation.

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Metabolism/Metabolites
In rabbits, the major end product of (14)C-ethylene glycol metabolism is carbon dioxide (60% of the dose within 3 days), and the metabolites excreted in urine are unchanged ethylene glycol (10%) and oxalic acid (0.1%). Glycol aldehydes, glycolic acid, and glyoxylic acid are intermediate products in the conversion to carbon dioxide.
In mammalian oxidative metabolism of ethylene glycol, there are species differences, which explain the differences in toxicity. Ethylene glycol is oxidized to carbon dioxide primarily via one pathway and to oxalic acid via a secondary pathway. The extent of oxalic acid formation depends on the dose level but has been shown to vary by species…
The initial steps of ethylene glycol oxidation to dialdehyde (glyoxal) and glyoxylic acid appear to be mediated by alcohol dehydrogenases; glyoxylic acid is decarboxylated to produce carbon dioxide and formic acid. Glyoxylic acid is also oxidized to oxalic acid.
Pyridoxine salts are complexes of glyoxylic acid and pyridoxine, in which pyridoxine is thought to promote the conversion of glyoxylic acid to glycine rather than oxalic acid in vivo. However, recent studies have shown that long-term use of pyridoxine may lead to excessive oxalate production and calcium oxalate kidney stones. There has been a previously unreported case of a patient developing both calcium oxalate kidney stones and chronic oxalate nephropathy with renal insufficiency after taking pyridoxine. Therefore, pyridoxine should be included in the list of chemicals that can cause chronic oxalate nephropathy. Cyclosporine A interferes with oxalate metabolism; therefore, it should be used with extreme caution in patients with primary hyperoxaluria. Oxalate is not metabolized but excreted in the urine.

Toxicity Summary
The affinity of divalent metal ions is sometimes manifested in their tendency to form insoluble precipitates. Therefore, in vivo, oxalic acid can also bind to metal ions such as Ca2+, Fe2+, and Mg2+, depositing corresponding oxalate crystals, thereby irritating the intestines and kidneys. (2) Thus, the toxicity of oxalic acid is due to renal failure caused by the precipitation of solid calcium oxalate (the main component of kidney stones). Oxalic acid can also cause joint pain due to the formation of similar precipitates in the joints. Ingestion of ethylene glycol produces oxalic acid metabolites, which can also lead to acute renal failure. Interactions Some thiol compounds have been shown to inhibit the process of glyoxylate generating CO2 and oxalate in rat liver homogenates and hepatocytes. Among them, cysteine has the most significant inhibitory effect, and this inhibitory effect is concentration-dependent. In rats with hyperoxaluria induced by the addition of ethylene glycol to drinking water, daily intraperitoneal injection of cysteine rapidly and significantly reduced urinary oxalate excretion, and this reduction persisted throughout the treatment period (28 days). During this period, urinary oxalate excretion in these glycol-treated rats decreased to control levels. This reduction is presumably due to the formation of the cysteine-glyoxylate adduct 2-carboxy-4-thiazolidinyl ester, which prevents further oxidation of glyoxylate to oxalate. Therefore, cysteine or similar thiol compounds may have potential as therapeutic agents for the prevention of kidney stones. This study aimed to investigate the effects of vitamin A, B1, and B6 deficiencies on oxalate metabolism in rats. Significant hyperoxaluria was observed in all three vitamin deficiencies (more prevalent in vitamin B6 deficiency than vitamin A, and more prevalent in vitamin A deficiency than vitamin B1). The activities of hepatic glycolate oxidase and glycolate dehydrogenase were significantly enhanced in vitamin A and vitamin B6-deficient rats. However, lactate dehydrogenase levels were not altered in these deficient rats compared to their respective paired-feeding controls. Four weeks of vitamin B1 deficiency only enhanced glycolate oxidase activity, while the levels of glycolate dehydrogenase and lactate dehydrogenase remained unchanged. Studies on intestinal oxalate absorption have shown that the bioavailability of oxalate in the intestines of rats deficient in vitamin A and vitamin B6 is increased. Therefore, the results indicate that both exogenous and endogenous oxalate play important roles in stone formation under various nutritional stress conditions. For patients undergoing regular hemodialysis, vitamin C supplementation may exacerbate hyperoxalemia. This study aimed to experimentally verify the validity of the above observations. Fifty rats with 5/6 nephrectomy were divided into two groups: 30 rats had free access to water containing 8 mg/ml vitamin C (100-160 mg/100 g/24 hr), while the remaining rats drank tap water without vitamin C. Serum creatinine gradually increased and hematocrit gradually decreased in both groups, but there was no significant difference between the two groups. Plasma vitamin C, oxalate, and urinary oxalate levels were higher in the vitamin C-treated group than in the untreated group. Histological examination revealed glomerular and interstitial fibrosis, round cell infiltration, and renal tubular cyst formation. Oxalate deposition in the renal tubules was only found in rats receiving vitamin C treatment and with severely impaired renal function. No oxalate deposition was observed in untreated rats with the same degree of renal impairment. These results confirm previous clinical findings that vitamin C supplementation exacerbates secondary oxalate deposition in chronic renal failure. Male Wistar rats fed a glycolic acid diet developed severe nephrocalcinosis and urinary calculi within 4 weeks. However, rats fed the same diet supplemented with citrate showed only mild or no nephrocalcinosis, and no urinary tract stones. The degree of nephrocalcinosis in the citrate group was intermediate between that in the citrate and glycolic acid groups, accompanied by a small number of urinary tract stones. During the experiment, urinary oxalate concentrations were significantly elevated, and both the citrate and glycolic acid groups had higher concentrations than the glycolic acid group. Urinary citrate concentrations in the citrate group were significantly higher than in other groups, while those in the citrate and glycolic acid groups were significantly lower than in other groups. Therefore, despite a slight increase in urinary oxalate, citrate can still inhibit nephrocalcinosis and stone formation by increasing urinary citrate levels and reducing urine saturation. For more complete data on interactions of oxalic acid (6 types in total), please visit the HSDB record page.

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Non-human toxicity values
Dog oral LDLo 1000 mg/kg

[1]. Oxalic acid, a pathogenicity factor for Sclerotinia sclerotiorum, suppresses the oxidative burst of the host plant. Plant Cell. 2000 Nov;12(11):2191-200.

Oxalic acid is an odorless white solid that sinks to the bottom when dissolved in water. (US Coast Guard, 1999)
Oxalic acid is an α,ω-dicarboxylic acid formed by replacing ethane with carboxyl groups at the 1 and 2 positions. It is found in humans, plants, and algae as a metabolite. It is the conjugate acid of oxalate (1-) and oxalate.
Oxalic acid is a metabolite found or produced in Escherichia coli (K12 strain, MG1655 strain).
Oxalic acid has also been reported in tea trees, microgreen algae, and some other organisms with relevant data.
Oxalic acid is a dicarboxylic acid, a colorless crystalline solid that forms a colorless acidic solution when dissolved in water. Its acidity is much stronger than acetic acid. Due to its dicarboxylic acid structure, oxalic acid can also act as a chelating agent for metal cations. Approximately 25% of oxalic acid is used as a mordant in dyeing processes. It is also used in bleaching, particularly in pulpwood. Oxalic acid's main uses include cleaning (it's also found in baking powder) and bleaching, especially for removing rust. Oxalic acid is present in many common foods, with spinach being particularly high in oxalates. Beetroot leaves, parsley, chives, and cassava are also quite rich in oxalates. Rhubarb leaves contain about 0.5% oxalic acid, while Arisaema triphyllum contains calcium oxalate crystals. Bacteria naturally produce oxalates through the oxidation of carbohydrates. In the human body, at least two enzymatic pathways exist for the synthesis of oxalates. In one metabolic pathway, oxaloacetate (part of the citric acid cycle) is hydrolyzed by oxaloacetase to oxalic acid and acetic acid. Oxalic acid can also be produced by the dehydrogenation of glycolate, which is produced by the metabolism of ethylene glycol. Oxalic acid is a competitive inhibitor of lactate dehydrogenase (LDH). LDH catalyzes the conversion of pyruvate to lactate while oxidizing the coenzyme NADH to NAD+ and H+. Because cancer cells preferentially utilize aerobic glycolysis, inhibiting LDH has been shown to suppress tumor formation and growth. However, oxalic acid is not particularly safe and is considered a mild toxicant. Of particular note is its well-known uremic toxin. In humans, the lowest known lethal oral dose of oxalic acid is 600 mg/kg. Lethal oral doses of oxalic acid have been reported to be 15 to 30 grams. Oxalic acid toxicity is due to kidney failure caused by the precipitation of calcium oxalate (a major component of kidney stones). Oxalic acid can also cause joint pain because similar deposits can form in the joints. Oxalic acid is a strong dicarboxylic acid found in many plants and vegetables. It is produced in the body by the metabolism of glyoxylic acid or ascorbic acid. It is not metabolized but excreted in the urine. It is used as an analytical reagent and a general reducing agent. See also: Oxalic acid dihydrate (active part); Sodium oxalate (the active ingredient)... See more...

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Mechanism of Action
From a metabolic perspective, its toxicity is thought to be due to oxalic acid's ability to fix calcium, thereby disrupting the calcium-potassium ratio in key tissues.

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Drug Warning
High doses of ascorbic acid in dialysis patients can lead to oxalate deposition in tissues. /oxalate/

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Oxalic acid is a key pathogenic factor secreted by Sclerotinia sclerotiorum. Its secretion is essential for successful infection. [1]
The mechanism by which oxalate enhances fungal virulence is thought to be the suppression of the host plant's oxidative burst (an early defense response). This effect is largely independent of simply lowering extracellular pH or chelating Ca²⁺. [1]
Some plants, such as wheat and barley, express oxalate oxidase, which degrades oxalate and produces H₂O₂, which may help resist oxalate-secreting pathogens. [1]

C2H2O4

90.0349

89.995

144-62-7

971

White to off-white solid powder

1.8±0.1 g/cm3

365.1±25.0 °C at 760 mmHg

189.5 °C (dec.)(lit.)

188.8±19.7 °C

0.0±1.7 mmHg at 25°C

1.480

-1.19

2

4

1

6

71.5

0

MUBZPKHOEPUJKR-UHFFFAOYSA-N

InChI=1S/C2H2O4/c3-1(4)2(5)6/h(H,3,4)(H,5,6)

oxalic acid

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~130 mg/mL (~1443.96 mM)

Solubility in Formulation 1: 3.25 mg/mL (36.10 mM) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 32.5 mg/mL clear DMSO stock solution to 400 μL of PEG300 and mix evenly; then add 50 μL of Tween-80 to the above solution and mix evenly; then add 450 μL of normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 3.25 mg/mL (36.10 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 32.5 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 3.25 mg/mL (36.10 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 32.5 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)