Toxicological assessment of sodium benzoate in Drosophila melanogaster.

Sodium benzoate (SB), the sodium salt of benzoic acid, is a food preservative with wide applications in the food, cosmetic and pharmaceutical industries due to its ability to kill many microorganisms effectively. Experimental evidence however suggests that excessive intake of SB poses detrimental health risks among consumers in the population. The present study investigated the toxic effects of various concentrations of SB using Drosophila melanogaster as a model. Adult wild-type flies of Canton S strain (1- to 3-days old) was orally exposed to SB (0, 0.5, 1.0, 2.0 and 5.0 mg/5 g diet) to evaluate survival rates for 21 days. Thereafter, we evaluated markers of oxidative stress, antioxidant status and behavioral activity in D. melanogaster exposed to SB for seven (7) days. We observed that SB (2.0 and 5.0 mg/5 g diet) decreased the survival of D. melanogaster. Also, SB inhibited glutathione-S-transferase activity and depleted total thiols and nonprotein thiols contents. Moreover, SB (5 mg/5 g diet) increased nitric oxide (nitrite/nitrate) level and reduced flies' emergence rate. Conclusively, findings from this study revealed that exposure to high concentrations of SB reduced survival rate and induced toxicity via the induction of oxidative stress and inhibition of antioxidant enzymes in D. melanogaster.

Sodium benzoate induces neurobehavioral deficits and brain oxido-inflammatory stress in male Wistar rats: Ameliorative role of ascorbic acid.

BACKGROUND: Sodium benzoate (SB) is a widely used food preservative. However, excessive intake of a high dose of SB poses a risk of neurotoxicity. Ascorbic acid (AA) is a naturally occurring antioxidant found in fruits with reported neuroprotective properties. The present study investigated the neurobehavioral and biochemical alterations in SB-treated rats and the ameliorative effect of AA in rats. METHODS: Forty-two male Wistar rats were divided into six groups (n = 7). Group 1 (vehicle, 10 ml/kg), Groups 2-4 rats SB (150, 300, and 600 mg/kg), Group 5 AA (100 mg/kg) and Group 6 (SB 600 mg/kg + AA 100 mg/kg). Treatment was daily administered for 28 days by oral route. Anxiogenic behavior, locomotor, and exploratory activities were evaluated in the open field monitored with a camera, and memory performance in Y-maze. Brain oxidative stress, inflammatory, apoptosis, and cholinergic markers were determined. The cortico-hippocampal tissues were examined histologically. RESULTS: SB-treated rats showed significant anxiogenic-like behavior and impairment in locomotor, exploratory, and memory performance. This was reversed in SB (600 mg/kg)-treated rats coadministered with AA. SB-treated rats showed a decrease in antioxidant enzyme activities, increase malondialdehyde (MDA), nitrite, tumor necrosis factor-alpha, caspase-3, and acetylcholinesterase activity in the striatum, hippocampus, frontal cortex, and cerebellum. These biochemical changes were reversed in AA-treated rats. Reduced cortico-hippocampal neuronal cell count and the pyknotic index were found in SB-treated rats, which was also reversed in AA-treated rats. CONCLUSION: Conclusively, sodium-benzoate-induced neurobehavioral deficits and brain biochemical changes were ameliorated by ascorbic acid probably via antioxidant, anti-inflammatory, and apoptotic mechanisms.

Protective role of protocatechuic acid in carbon tetrachloride-induced oxidative stress via modulation of proinflammatory cytokines levels in brain and liver of Wistar rats.

OBJECTIVES: Protocatechuic acid (PCA) possesses numerous pharmacological activities, including antioxidative and anti-inflammatory activities. This study seeks to investigate its underlying mechanism of action in the liver and brain toxicity induced by CCl4 in male albino rats. METHODS: Rats were given PCA at 10 and 20 mg/kg daily and orally as a pretreatment for seven days. A single injection of CCl4 was given 2 h later to induce brain and liver toxicity. RESULTS: CCl4 moderately elevated the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP). PCA lowered AST level significantly when compared to control. Total protein and albumin levels presented insignificant changes (p>0.05) in all groups while lipid profile showed increased total cholesterol level and reduced high-density lipoprotein (HDL) by CCl4. PCA (10 mg/kg) significantly reduced the cholesterol level while the 20 mg/kg dose moderately prevented HDL reduction. There was an increased MDA production with a corresponding low GSH level in the group treated with CCl4. Activities of superoxide dismutase, catalase, and glutathione-S-transferase in both organs also declined. PCA, especially at 10 mg/kg attenuated lipid peroxidation by increasing GSH level in the organs. Biochemical assays revealed the improvement of antioxidant enzyme activities by PCA in these organs. Furthermore, PCA lowered the level of proinflammatory cytokine COX 2 in the brain and liver while NF-kB expression was inhibited in the brain. Histopathology reports validated the effects of PCA. CONCLUSIONS: PCA exhibited protection against toxicity in these tissues through antioxidant and anti-inflammatory activities and the potential mechanism might be through modulation of the NF-κB/COX-2 pathway.

Chrysophyllum albidum fruit peel attenuates nociceptive pain and inflammatory response in rodents by inhibition of pro-inflammatory cytokines and COX-2 expression through suppression of NF-κB activation.

Chrysophyllum abidum fruit is a seasonal fruit commonly eaten as snacks with abundant health promoting phytochemicals in the fruit peels. The fruit peels have been reported to be rich in anti-inflammatory eleagnine, myricetin rhamnoside, quercetin, linoleic acid and oleic acid. We hypothesized that the anti-inflammatory effect of the peel extract involve suppression of pro-inflammatory cytokines, cyclooxygenase-2 and nuclear factor-kappa B (NF-κB). Hence, this study was designed to assess the anti-nociceptive and anti-inflammatory effects of fruit peel extract of Chrysophyllum albidum in animal models of nociception and inflammation. The anti-nociceptive activity of CAPEE (100 and 400 mg/kg) was evaluated in acetic acid-induced writhing and formalin-induced paw licking in mice. Formalin-induced paw edema and carrageenan-induced air pouch models of inflammation were used to evaluate the anti-inflammatory activity. CAPEE (100 and 400 mg/kg) significantly reduced abdominal writhing and paw licking in acetic acid and formalin tests in mice, respectively. CAPEE demonstrated significant inhibition of paw edema at 24 h (41.0% and 55.7%) and 72 h (52.3% and 86.6%) after formalin injection. CAPEE suppressed inflammatory responses in carrageenan-induced air pouch by reducing exudates, inflammatory cells infiltration, nitrites and myeloperoxidase activity. There was significant inhibition of tumor necrosis factor-alpha, interleukin-6 levels and reduced immunopositive expression of COX-2 and NF-κB. In conclusion, CAPEE has anti-nociceptive and anti-inflammatory potentials via mechanisms associated with inhibition of pro-inflammatory cytokines and cyclooxygenase-2 (COX-2) expression through suppression of nuclear factor kappa B (NF-κB) activation, and has potential as a functional food ingredient.