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At least 19 recordsLinked to original sources
PubMed2004

[Studies for analyzing restricted ingredients such as sodium benzoate].

Sodium benzoate is a kind of preservatives in cosmetics and is nominated as the restricted ingredients in cosmetics in Japanese Pharmaceutical Affairs Act. So the analytical method for sodium benzoate was investigated by HPLC. After adding 5 ml of tetrahydrofuran to 0.05 g of the lotions or creams with 0.1 or 1.0% sodium benzoate and dissolving them, that mixture was made up to 50 ml with methanol. If necessary, the mixture was filtrated with a membrane filter (0.45 microm). The testing solution of 20 micro1 was analyzed by HPLC using the ODS column (CAPCELL PAK C18 column, 4.6 x 250 mm), the mixture of 50 mmol/l phosphate buffer (pH5.5) and acetonitrile (7:3) and the detection wavelength of 227 nm. The working curve from 1.0 to 12.0 microg/ml showed a linear line between the concentrations of sodium benzoate and the peak area. There was no interference of peak of sodium benzoate from the lotion and cream.

Acetonitriles↗
PubMed2000

Three cases of intravenous sodium benzoate and sodium phenylacetate toxicity occurring in the treatment of acute hyperammonaemia.

Intravenous sodium benzoate and sodium phenylacetate have been used successfully in the treatment of acute hyperammonaemia in patients with urea cycle disorders. They provide alternative pathways for waste nitrogen disposal and help maintain nitrogen homeostasis. However, we report three patients with hyperammonaemia who received inappropriate doses of intravenous sodium benzoate and sodium phenylacetate that resulted in severe complications. Ambiguous medical prescriptions and inadequate cross-checking of drug dosage by physicians, nurses and pharmacists were the main causes of these incidents. All the patients presented with alteration in mental status, Kussmaul respiration and a partially compensated metabolic acidosis with an increased anion gap. Two patients developed cerebral oedema and hypotension and died. The third survived after haemodialysis. Plasma levels of benzoate and phenylacetate were excessively high. The possible mechanisms of toxicity, management and safety measures are discussed.

Child↗
PubMed1989

Carbamyl glutamate prevents the potentiation of ammonia toxicity by sodium benzoate.

Sodium benzoate has been recommended for the treatment of hyperammonaemia in humans. However, benzoate potentiates ammonia toxicity and reduces urea synthesis in vitro and in vivo by decreasing the intramitochondrial levels of N-acetyl glutamate. Pretreatment of mice with carbamyl glutamate, a structural analogue of N-acetyl glutamate, decreases mortality induced by ammonium acetate and sodium benzoate administration. The protective effect of carbamyl glutamate is accompanied by an increase in urea production and of carbamyl phosphate synthetase activity.

Ammonia↗
PubMed1988

Effect of sodium benzoate and sodium phenylacetate on brain serotonin turnover in the ornithine transcarbamylase-deficient sparse-fur mouse.

Herein we examine the effects of sodium benzoate and sodium phenylacetate on feeding and central serotonin turnover in a child with citrullinemia and in an animal model of congenital hyperammonemia, the ornithine transcarbamylase-deficient sparse-fur (spf/y) mouse. In the child, when the benzoate/phenylacetate dosage was increased from 200 to 375 mg/kg/day each, feeding decreased. There was an accumulation of benzoate and phenylacetate in blood and cerebrospinal fluid as well as an increased concentration of 5-hydroxyindoleacetic acid, a neurochemical marker for serotonin turnover, in cerebrospinal fluid. In the mouse, sodium benzoate had a biphasic effect on both plasma ammonium levels and brain serotonin turnover. Two percent oral benzoate was associated with an increase in ammonium level, while a 3% dose led to a decrease in ammonium. There was a similar effect on serotonin turnover noted in both the hyperammonemic spf/y and control CD-1/y mice. Sodium phenylacetate did not have a consistent effect on serotonin turnover. The mechanism by which benzoate increases brain serotonin turnover appears to involve competition with tryptophan for albumin binding sites. This results in increased free tryptophan in serum and brain. We speculate that some of the clinical symptoms of benzoate intoxication may be a consequence of altered serotonin turnover in the brain. We suggest that drug levels be monitored during therapy.

Administration, Oral↗
PubMed1993

Effect of a sodium benzoate-sodium bicarbonate compound on dental plaque formation.

The objective of this study was to evaluate the effect of a sodium benzoate-sodium bicarbonate (SBSB) compound on dental plaque formation and developing gingivitis. Eighteen subjects were given a prophylaxis and instruction in oral hygiene to establish plaque-free conditions and gingival health for the study baseline. They were randomly divided into three groups. Each participant was instructed to rinse twice daily with either a 0.15% chlorhexidine digluconate solution, the SBSB compound, or a placebo solution for 21 days. They refrained from all other oral hygiene procedures during this period. Plaque, gingival, and stain indices were scored at baseline and at days 7, 14, and 21 during the rinsing protocol. A significant increase in plaque accumulation was observed for the SBSB compound and placebo groups in days 7 through 21. No increase in plaque accumulation was observed in the chlorhexidine group. An increase in gingival inflammation was observed in all groups, with no significant differences between groups. Significant increases in gingival bleeding occurrence compared to baseline were found in the chlorhexidine group by day 21, in the SBSB compound group by day 7, and in the placebo group by day 14. The present study did not disclose any plaque or gingivitis inhibiting effects of the SBSB compound.

Adult↗
PubMedDate not supplied

Cytogenetic effects of the food preservatives--sodium benzoate and sodium sulphite on Vicia faba root meristems.

Sodium sulphite and sodium benzoate induce in Vicia faba root meristems: (1) dose-dependent reduction in mitotic figures, (2) intact and severed anaphase bridges, (3) premature chromosome condensation heading to pycnotic nuclei, and (4) chromatin erosion in interphase nuclei. The effects are due to the anions and not due to the sodium ions. Complete recovery of mitotic figures and normal chromosome configurations were observed within the first 23-46 h of regrowth. Recovery was accompanied by severed anaphase bridges and micronuclei of various shapes. Both benzoate and sulphite inhibit DNA synthesis in Vicia faba root meristems. Sulphite was more effective than benzoate.

Benzoates↗
PubMed1997

[Determination of caffeine and sodium benzoate contents in caffeine and sodium benzoate injection by P-matrix method].

The contents of caffeine and sodium benzoate injection may be determined by P-matrix method without separation of its components. BSAIC language is used for programming. The average recovery of caffeine is 100.0% and that of sodium benzoate is 99.95%. The variation coefficient of caffeine is 0.40% and that of sodium benzoate is 0.65%. On the basis of recovery rate and data observed it is concluded that this method is accurate, reliable, simple and rapid as compared with the standard pharmacopoeia regulations.

Caffeine↗
PubMed1980

Report of carcinogenesis bioassay of sodium benzoate in rats: absence of carcinogenicity of sodium benzoate in rats.

The carcinogenicity of sodium benzoate was examined in Fischer 344 rats. Sodium benzoate was administered in the diet for 18 to 24 months at two dose levels; concentrations of 2% and 1% in the diet, which corresponded to the maximum tolerated dose (MTD) and 1/2 MTD as estimated from the data obtained by 6-week toxicity study. Fifty males and 52 females each were used per group. Controls consisted of 25 male rats and 43 female rats. No adverse clinical signs directly attributable to the compound were observed in treated animals. Differences in the average body weight, and mortality rates between treated and control groups were negligible. The results of the statistical test for dose-related trends were not significant (p < 0.05) Although a variety of tumors occurred among test and control rats of each sex, tumors appearing in treated rats were similar in type and number to those in controls. It was concluded that no evidence of carcinogenicity in rats from sodium benzoate was demonstrated.

Animals↗
PubMed1988

Mitochondrial urea cycle enzymes in rats treated with sodium benzoate.

Since sodium benzoate, which is widely used to treat hyperammonemia its effect on mitochondrial urea cycle enzymes was investigated. its effect on mitochondrial urea cycle enzymes was investigated. Sodium benzoate was administered to urease treated hyperammonemic rats and controls. In both groups no interference with the activity of carbamylphosphate synthetase, ornithine carbamyltransferase and N-acetylglutamate synthetase in the liver could be observed at concentrations of benzoate in plasma found in hyperammonemic patients. Careful monitoring of plasma levels reduces benzoate toxicity as shown in a patient with argininosuccinic aciduria.

Acetyltransferases↗
PubMed1993

[Profile of hepatic and muscular acylcarnitines in chronically hyperammonemic mice after an acute treatment with sodium benzoate: dose-response study].

Sodium benzoate is conjugated with glycine in the liver and the kidney, which may cause the elimination of one mole of alpha-amino N for each mole of benzoate administered. However, muscle does not possess the enzyme activity to form benzoylglycine. The object of this study was to identify the secondary effects of acute sodium benzoate treatment on the concentrations of carnitine in liver and muscle when the glycine availability in these tissues is still assured. Our studies are based on chronically hyperammonemic spf/Y mice with a deficiency of ornithine transcarbamylase. The animals were given 2.5, 5.0 and 10.0 mmol/kg sodium benzoate intraperitoneally. Control groups of normal mice received identical treatments. Our results demonstrate that sodium benzoate influences the homeostasis of liver and muscle carnitine after only 15 minutes of treatment. We observed a reduction of short- and medium-chain acylcarnitines in the liver of normal mice, and an increase of free carnitine and long-chain acylcarnitines in the spf mice. In muscle, we found a reduction of free carnitine and short- and medium-chain acylcarnitines at doses of 5.0-10.0 mmol benzoate/kg in the normal mice. However, we observed a significant reduction of long-chain acylcarnitines in muscle tissue from spf mice. The carnitine concentrations in each tissue differ depending on the dose of sodium benzoate administered, which may suggest a biphasic effect. Our results indicate that sodium benzoate has a secondary effect on the liver and muscle concentration of carnitine from the beginning of its intramitochondrial metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcarnitine↗
PubMed1983

Effect of sodium benzoate on polymorphonuclear leukocyte function.

Sodium benzoate is widely used as a food preservative and reputed to be a scavenger of hydroxyl radical (.OH). The effects of sodium benzoate on the function of polymorphonuclear leukocytes (PMN) stimulated by S. aureus or the chemical agent, phorbol myristate acetate (PMA) were examined in vitro using assays of chemiluminescence (CL), total bactericidal activity, intracellular recovery of bacteria, as well as release of lactate dehydrogenase (LDH), lysozyme and superoxide anion (O2(-)). Sodium benzoate decreased chemiluminescence, superoxide anion and lysozyme release by PMN stimulated with S. aureus but did not similarly affect these responses of PMN to the chemical agent, PMA. The ability of PMN to kill S. aureus was also impaired by sodium benzoate and associated with a reduced number of intracellular bacteria recovered after 90 minutes incubation. LDH release from PMN was not demonstrable at concentrations of sodium benzoate below 100 mM indicating that damage can not account for these findings. The underlying mechanism of the altered bactericidal function of PMN treated with sodium benzoate appears to be a result of decreased uptake of S. aureus.

Adult↗