Zero-valent magnesium (ZVMg), glacial acetic acid (GAA), and vitamin B₁₂ were used to degrade trichloroethylene (TCE) in either pure anhydrous ethanol (EtOH) or 10% anhydrous EtOH in canola oil. Gas chromatography–mass spectrometry (GC–MS) was used to monitor the decrease in TCE concentration within each system over time. In pure anhydrous EtOH, a vitamin B₁₂ concentration of 49.2 mg/L achieved the highest decrease in TCE concentration by 96 ± 0.4% (with lower vitamin B₁₂ concentration, degradation was lower). Vitamin B₁₂ and ZVMg also performed synergistically, increasing TCE degradation by approximately 78% relative to either ZVMg or vitamin B₁₂ alone. In pure anhydrous EtOH, with ZVMg and vitamin B₁₂, TCE was below detection after 2 h. Degradation products were likely volatile, as they were not detected in all liquid samples. Spectrophotometric analyses indicated the formation of the super reducing species of vitamin B₁₂ (i.e., Co(I)) after 30 min in the presence of ZVMg, explaining the significant increase in TCE degradation. TCE degradation was also tested in 10% anhydrous EtOH in canola oil, with the purpose of developing a formulation for the in situ remediation of TCE-polluted aquifers. Canola oil would promote ZVMg contact with TCE, while mitigating its oxidation due to contact with groundwater. In 10% anhydrous EtOH in canola oil, the concentration of TCE decreased by approximately 40% within 30 min, with ZVMg alone. Our study provides the first proof of concept of an efficient in situ remediation method using environmentally friendly reagents, such as vitamin B₁₂ and canola oil, for the degradation of TCE in polluted aquifers.

Polycyclic aromatic hydrocarbons (PAHs) are environmental chemicals that are formed due to incomplete combustion of the organic matters, or during heat treatment of the food. The objectives of the present study were first to estimate levels of the 15-priority PAHs in the edible vegetable oil (corn oil, sunflower oil, olive oil, and canola oil) collected from Egypt. Furthermore, the effect of heat treatment on the formation of PAHs in the canola oil was further examined. In addition, dietary intakes and cancer risk among Egyptian consumers were additionally calculated. The achieved results indicated presence of 15-priority PAHs in all examined oil samples. Canola oil had the highest residual concentrations of PAHs compared with the other tested oil species. Heat treatment of canola oil led to a drastic increase in the formed B[a]P (316.55%), total 2-PAHs (322.47%), total 4-PAHs (297.42%), total 8-PAHs (285.26%), and total 15-PAHs (443.32%), respectively. The incremental lifetime cancer risk among the Egyptian population is considered safe when was calculated for all examined oil samples.

This study investigated the protective effects of melatonin (MLT), a potent antioxidant, in male Wistar rats exposed to environmentally relevant doses of bisphenol A (BPA) in utero. Pregnant Wistar rats were randomly assigned into five groups. Group 1 (control) received 0.2 mL 1% dimethyl sulfoxide (DMSO)/99% canola oil as vehicle; group 2 received BPA at 25 μg/kg/day; group 3 received BPA at 250 μg/kg/day; group 4 received BPA at 25 μg/kg/day with concurrent MLT 1 mg/kg/day while group 5 received BPA at 250 μg/kg/day with concurrent MLT 1 mg/kg/day. Treatments were by gavage from gestational day (GD) 10–21. The BPA-treated rats showed dose-dependent significant reduction in body weight, gonosomatic index, sperm motility, livability and count. Also, BPA caused significant reduction in the levels of serum testosterone and luteinizing hormone while it caused significant increases in the levels of follicle stimulating hormone as well as estradiol. Furthermore, BPA induced testicular oxidative stress including significant decreases in the activities of testicular SOD, GSH and GPx as well as GST, increasing the levels of testicular MDA and H₂O₂. It further induced interstitial necrosis and germinal cell degeneration in the testis with a subsequent diminution of the tubular and luminal diameter. However, co-treatment with MLT offered protection against testicular damage induced by BPA. Melatonin is likely to protect against alterations of the male reproductive system caused by BPA through a direct action on the mechanism of anti-oxidants as well as through the inhibition of necrosis.

Recently, biodiesel production using heterogeneous catalysts has been of great concern. However, simple separation of these catalysts from product mixtures is a problem of the process. In this study, series of magnetic KOH/Fe₃O₄@Al₂O₃ core–shell nanocatalysts were synthesized via the incipient wetness impregnation method and the effect of weight ratio of Fe₃O₄-to-Al₂O₃ (0.15–0.35) on the catalytic performance was assessed. The samples were characterized by XRD, FTIR, BET-BJH, VSM, SEM, TEM, and EDX analyses and their basicity was measured by the Hammett indicator method. The results revealed that although the magnetic KOH/Fe₃O₄@Al₂O₃ nanocatalyst with 25 wt% of Fe₃O₄ showed less activity as compared to those with 15 wt% of Fe3O4, it exhibited higher surface area and appropriate magnetic properties. The sample presented superparamagnetic properties with the magnetic strength of 1.25 emu/g that was simply recovered by using an external magnetic field. The nanocatalyst converted 98.8% of canola oil to biodiesel under reflux condition at the best operational conditions of 12 M ratio of methanol/oil, 4 wt% of catalyst and 6 h of reaction time. Moreover, the nanocatalyst showed high reusability such that it was reused several times without appreciable loss of its catalytic activity.

The prevalence of aflatoxins (AFs) B₁, B₂, G₁, and G₂ in Iranian edible oils were assessed by immunoaffinity column cleanup and HPLC equipped with a fluorescence detector (HPLC-FLD). Ninety-seven samples including sunflower, canola, refined olive, unrefined olive, frying, and blend oils were collected from eight provinces (n = 15 samples of refined olive oil, n = 15 samples of unrefined olive oil, n = 15 samples of sunflower oil, n = 15 samples of canola oil, n = 17 samples of frying oil, and n = 20 samples of blend oil). Also, cancer risk of aflatoxins in the adults and children due to ingestion of edible oils was estimated via margin of exposure (MOE) estimation in the Monte Carlo simulation (MCS) model. Considering the limit of detection (LOD) of the current study, two unrefined olive oil samples from Zanjan Province were contaminated with AFB₂ in the concentrations of 0.2 and 0.4 ng/g while other samples were free from AFB₁, AFB₂, AFG₁, and AFG₂. This study revealed that about 98% of the collected samples were free from AFs and the concentrations of AFs in the polluted samples were within the standard range suggested by European Commission regulation (20 μg/kg). However, health risk assessment indicated that both adult and children in the Zanjan Province are at considerable liver cancer risk (percentile 95% of MOE < 10,000 value). Therefore, national plan to address this issue and strict inspection of edible oil products by the regulatory bodies are suggested.

This study investigated the role of melatonin (MLT) on adrenal gland toxicity induced by bisphenol A (BPA). Adult male rats were divided into four groups of seven animals each: Group I (control) received oral 0.2 ml canola oil; group II received intra-peritoneal 10 mg/kg BW/day MLT; and group III received oral BPA (10 mg/kg BW/day). Group IV rats were treated with same dose of BPA as group III with a concomitant intra-peritoneal 10 mg/kg BW/day MLT. All treatments lasted for 14 days. BPA significantly increased (P < 0.05) adrenal index, circulating levels of corticosterone and adrenocorticotropic hormone (ACTH) in the rats. BPA caused marked vascular congestion, hyperplasia, cellular distortion, increased lipid peroxidation, decreased antioxidant enzymes, and decreased expression of αSmooth muscle actin as well as vimentin proteins. The concomitant treatment with MLT ameliorated these BPA-induced alterations. It is likely that melatonin attenuates BPA-induced alterations of the adrenal gland of rats through the antioxidant defense mechanism.