Citric acid

The herbs of Saccharum sinense

Citric acid is a weak organic tricarboxylic acid found in citrus fruits. Citric acid is a natural preservative and food tartness enhancer.

In Vitro:Citric acid induces apoptosis through the mitochondrial pathway in the human keratinocyte cell line HaCaT. It inhibits proliferation of HaCaT cells in a dose-dependent manner, but also induces apoptosis and cell cycle-arrest at the G2/M phase (before 24 h) and S phase (after 24 h)[1].

In Vivo:Citric acid is found in all animal tissues as an intermediary substance in oxidative metabolism. The administration of citric acid (1–2 g/kg) attenuates LPS-induced elevations in brain MDA, nitrite, TNF-α, GPx, and PON1 activity. In the liver, nitrite is decreased by 1 g/kg citric acid. Citric acid (1-2 g/kg) decreases brain lipid peroxidation and inflammation, liver damage, and DNA fragmentation[2]. Citric acid supplementation increases intestinal calcium and phosphorus absorption and the retention/intake ratio only in rats fed the 1% Ca diet. Citric acidsupplementation together with a calcium-rich diet allows to obtain an increased retention of calcium and phosphorus in bone. The prolonged administration of calcium citrate supplements may therefore help to increase bone mineral concentration[3]. Oral administration of citric acid ameliorates ketosis and protects against the development of diabetic complications in an animal model of type 1 diabetes[4].

References:
[1]. Ying TH, et al. Citric acid induces cell-cycle arrest and apoptosis of human immortalized keratinocyte cell line (HaCaT) via caspase- and mitochondrial-dependent signaling pathways. Anticancer Res. 2013 Oct;33(10):4411-20. [2]. Abdel-Salam OM, et al. Citric acid effects on brain and liver oxidative stress in lipopolysaccharide-treated mice. J Med Food. 2014 May;17(5):588-98. [3]. Lacour B, et al. Stimulation by citric acid of calcium and phosphorus bioavailability in rats fed a calcium-rich diet. Miner Electrolyte Metab. 1997;23(2):79-87. [4]. Nagai R, et al. Citric acid inhibits development of cataracts, proteinuria and ketosis in streptozotocin (type 1) diabetic rats. Biochem Biophys Res Commun. 2010 Feb 26;393(1):118-22.

The role of citric acid on the phytoremediation of heavy metal contaminated soil.[Pubmed:12688495]

Chemosphere. 2003 Feb;50(6):807-11.

Adsorption and hydroponics experiments were conducted to study the role of Citric acid on the phytoremediation of heavy metal contaminated soil. The results show that addition of Citric acid decreased the adsorption of both lead and cadmium, such an effect was bigger for cadmium than for lead. The decrease in the adsorption of Pb and Cd was mainly due to a decrease of pH in the presence of Citric acid. The presence of Citric acid could alleviate the toxicity of Pb and Cd to radish, and stimulate their transportation from root to shoot. The studies of heavy metal forms using sequential extraction demonstrated that lead was mainly existed as FHAC (a lower bioavailable form) in the root, while F(HCl) was the dominant form in the leaf. The addition of Citric acid to the soil changed the concentration and relative abundance of all the forms. The detoxifying effect of Citric acid to Pb in shoots might result from the transformation of higher toxic forms into lower toxic forms. Cadmium was mainly present as F(NaCl), therefore, it had higher toxicity than lead. The addition of Citric acid increased the abundance of F(H2O) + F(NaCl), indicating that Citric acid treatment could transform cadmium into more transportable forms.

Citric acid effects on brain and liver oxidative stress in lipopolysaccharide-treated mice.[Pubmed:24433072]

J Med Food. 2014 May;17(5):588-98.

Citric acid is a weak organic acid found in the greatest amounts in citrus fruits. This study examined the effect of Citric acid on endotoxin-induced oxidative stress of the brain and liver. Mice were challenged with a single intraperitoneal dose of lipopolysaccharide (LPS; 200 mug/kg). Citric acid was given orally at 1, 2, or 4 g/kg at time of endotoxin injection and mice were euthanized 4 h later. LPS induced oxidative stress in the brain and liver tissue, resulting in marked increase in lipid peroxidation (malondialdehyde [MDA]) and nitrite, while significantly decreasing reduced glutathione, glutathione peroxidase (GPx), and paraoxonase 1 (PON1) activity. Tumor necrosis factor-alpha (TNF-alpha) showed a pronounced increase in brain tissue after endotoxin injection. The administration of Citric acid (1-2 g/kg) attenuated LPS-induced elevations in brain MDA, nitrite, TNF-alpha, GPx, and PON1 activity. In the liver, nitrite was decreased by 1 g/kg Citric acid. GPx activity was increased, while PON1 activity was decreased by Citric acid. The LPS-induced liver injury, DNA fragmentation, serum transaminase elevations, caspase-3, and inducible nitric oxide synthase expression were attenuated by 1-2 g/kg Citric acid. DNA fragmentation, however, increased after 4 g/kg Citric acid. Thus in this model of systemic inflammation, Citric acid (1-2 g/kg) decreased brain lipid peroxidation and inflammation, liver damage, and DNA fragmentation.

The effects of citric acid on phytate-phosphorus utilization in young chicks and pigs.[Pubmed:10764076]

J Anim Sci. 2000 Mar;78(3):682-9.

Several bioassays were conducted with young chicks and pigs fed phosphorus (P)-deficient corn-soybean meal diets. With diets for chicks containing .62% Ca and .42% P (.10% available P), graded doses of a Citric acid + sodium citrate (1:1, wt:wt) mixture (0, 1, 2, 4, or 6% of diet) resulted in linear (P < .01) increases in both weight gain and tibia ash. Relative to chicks fed no Citric acid, tibia ash (%) and weight gain (g/d) were increased by 43 and 22%, respectively, in chicks fed 6% Citric acid. Additional chick trials showed that 6% Citric acid alone or sodium citrate alone was as efficacious as the Citric acid + sodium citrate mixture and that 1,450 U/kg of phytase produced a positive response in bone ash and weight gain in chicks fed a diet containing 6% citrate. Varying the Ca:available P ratio with and without citrate supplementation indicated that Citric acid primarily affected phytate-P utilization, not Ca, in chicks. Moreover, chicks did not respond to citrate supplementation when fed a P-deficient (.13% available P), phytate-free casein-dextrose diet. Young pigs averaging 10 to 11 kg also were used to evaluate Citric acid efficacy in two experiments. A P-deficient corn-soybean meal basal diet was used to construct five treatment diets that contained 1) no additive, 2) 3% Citric acid, 3) 6% Citric acid, 4) 1,450 U/kg phytase, and 5) 6% Citric acid + 1,450 U/kg phytase. Phytase supplementation increased (P < .01) weight gain, gain:feed, and metatarsal ash, whereas Citric acid addition increased only gain:feed (P < .05) and metatarsal ash (P < .08). A subsequent 22-d pig experiment was conducted to evaluate the effect of lower levels of Citric acid (0, 1, 2, or 3%) or 1,450 U/kg phytase addition to a P-deficient corn-soybean meal diet. Phytase supplementation improved (P < .01) all criteria measured. Weight gain and gain:feed data suggested a response to Citric acid addition, but this was not supported by fibula ash results (P > .10). The positive responses to phytase were much greater than those to Citric acid in both pig experiments. Thus, dietary Citric acid effectively improved phytate P utilization in chicks but had a much smaller effect in pigs.

Efficacy of citric acid denture cleanser on the Candida albicans biofilm formed on poly(methyl methacrylate): effects on residual biofilm and recolonization process.[Pubmed:24957210]

BMC Oral Health. 2014 Jun 23;14:77.

BACKGROUND: It is well known that the use of denture cleansers can reduce Candida albicans biofilm accumulation; however, the efficacy of Citric acid denture cleansers is uncertain. In addition, the long-term efficacy of this denture cleanser is not well established, and their effect on residual biofilms is unknown. This in vitro study evaluated the efficacy of Citric acid denture cleanser treatment on C. albicans biofilm recolonization on poly(methyl methacrylate) (PMMA) surface. METHODS: C. albicans biofilms were developed for 72 h on PMMA resin specimens (n = 168), which were randomly assigned to 1 of 3 cleansing treatments (CTs) overnight (8 h). CTs included purified water as a control (CTC) and two experimental groups that used either a 1:5 dilution of Citric acid denture cleanser (CT5) or a 1:8 dilution of Citric acid denture cleanser (CT8). Residual biofilms adhering to the specimens were collected and quantified at two time points: immediately after CTs (ICT) and after cleaning and residual biofilm recolonization (RT). Residual biofilms were analyzed by quantifying the viable cells (CFU/mL), and biofilm architecture was evaluated by confocal laser scanning microscopy (CLSM) and scanning electron microscopy (SEM). Denture cleanser treatments and evaluation periods were considered study factors. Data were analyzed using two-way ANOVA and Tukey's Honestly Significant Difference (HSD) test (alpha = 0.05). RESULTS: Immediately after treatments, Citric acid denture cleansing solutions (CT5 and CT8) reduced the number of viable cells as compared with the control (p < 0.01). However, after 48 h, both CT groups (CT5 and CT8) showed biofilm recolonization (p < 0.01). Residual biofilm recolonization was also detected by CLSM and SEM analysis, which revealed a higher biomass and average biofilm thickness for the CT8 group (p < 0.01). CONCLUSION: Citric acid denture cleansers can reduce C. albicans biofilm accumulation and cell viability. However, this CT did not prevent biofilm recolonization.

Citric acid is a weak organic tricarboxylic acid found in citrus fruits. Citric acid is a natural preservative and food tartness enhancer.

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