Oxalic Acid   中文名称: 草酸

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].

即使在没有其他真菌成分的情况下，草酸（菌核病的致病因子）也会抑制宿主植物的氧化爆发，并直接限制大豆细胞响应 OGA 合成 H2O2[1]。

---

在悬浮培养的烟草和大豆细胞中，草酸 能抑制由多种激发子诱导的氧化爆发（H₂O₂产生），半数抑制浓度约为4至5 mM，约在6-7 mM时达到最大抑制。它能抑制由寡聚半乳糖醛酸、轮枝菌激发子、低渗胁迫、斑蝥素和harpin蛋白诱导的爆发，但对harpin诱导爆发的最大抑制仅能达到对照的约30%。[1]
来自野生型产草酸核盘菌菌株（含~12.4 mM草酸）的培养滤液几乎完全抑制了烟草细胞中OGA诱导的H₂O₂产生，而来自草酸缺陷型突变体（含~0.11 mM草酸）的滤液则无此作用。向突变体滤液中添加11 mM草酸可恢复其抑制能力。[1]
抑制效应在很大程度上与培养基酸化或钙离子螯合无关。草酸不抑制水母发光蛋白转化的烟草细胞中激发子刺激的胞质钙离子瞬变。[1]
草酸仅在激发子激活前或早期阶段添加时才抑制氧化爆发；一旦H₂O₂产生达到最大速率后添加则无效，表明其作用于组装/激活的氧化酶复合体催化步骤之前。[1]

用草酸缺陷型、非致病性的核盘菌突变体接种烟草叶片，可诱导可测量的氧化爆发（通过氮蓝四唑染色可视化）；而用野生型产草酸菌株接种则不能。产草酸菌株能成功定殖叶片组织。[1]

H₂O₂产生测定： 通过荧光法测量染料pyranine（激发波长405 nm，发射波长512 nm）的氧化淬灭来监测植物悬浮细胞（烟草或大豆）中H₂O₂的产生。将1.5 mL细胞置于荧光比色皿中，加入1 µg/mL pyranine。加入激发子（如5 µg/mL OGA）后，通过测量荧光淬灭的最大速率来估算H₂O₂的生物合成速率。测试化合物如 草酸（pH调整至5.7）在激发子刺激时或指定时间后加入。数据以同日对照细胞速率的百分比表示。[1]
胞质钙离子测量： 使用发光测量法监测水母发光蛋白转化的烟草细胞中胞质钙离子浓度的变化。细胞在激发子（如OGA）刺激前5分钟用测试化合物（如10 mM草酸或1.5 mM BAPTA-AM）处理。记录发光值并将其转化为相应的钙离子浓度。每次运行后，通过用氯化钙和去污剂裂解细胞来定量残留的功能性水母发光蛋白。[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.

---

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.

---

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...

---

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.

---

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

---

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

74.6

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)

配方 1 中的溶解度: 3.25 mg/mL (36.10 mM) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 悬浮液；超声助溶。
例如，若需制备1 mL的工作液，可将100 μL 32.5 mg/mL澄清DMSO储备液加入到400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

---

配方 2 中的溶解度: ≥ 3.25 mg/mL (36.10 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 32.5 mg/mL 澄清 DMSO 储备液加入 900 μL 20% SBE-β-CD 生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

---

View More

配方 3 中的溶解度: ≥ 3.25 mg/mL (36.10 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 32.5 mg/mL 澄清 DMSO 储备液加入900 μL 玉米油中，混合均匀。

---

请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。