There is a growing concern over the food safety issue related to increased incidence of cooking oil adulteration with recycled cooking oil (RCO). The objective of this study was to detect fresh palm olein (FPO) adulteration with RCO using fatty acid composition (FAC) and Fourier-transform infrared spectroscopy (FTIR) spectral analyses combined with chemometrics. RCO prepared in the laboratory was mixed with FPO in the proportion ranged from 1% to 50% (v/v) to obtain the adulterated oil samples (AO). FACs for FPO, RCO, and AO were determined using gas chromatography equipped with a flame ionization detector (GC-FID). The compositions of most fatty acids in RCO lied within the normal ranges of Codex standard, except for C8:0, C10:0, C11:0, C15:0, trans C18:1, and polyunsaturated fatty acids (PUFAs), C20:5. PUFAs showed a consistent decreasing trend with increasing magnitude of change with respect to increasing adulteration level and thus might be a good indicator for detecting FPO adulteration with RCO. The evaluation parameters (coefficient of determination, root mean standard error) of the FTIR-partial least square (PLS) model of palm oil adulteration with recycled oil are R 2 = 0.995 and 3.25, respectively. For FTIR spectral analysis, the distinct variations in spectral regions and aberrations in characteristic bands between FPO and RCO were observed. The optimized PLS calibration model developed from normal spectral of the combined region at 3602-3398, 3016-2642, and 1845-650 cm −1 overpredict the adulteration level. On the other hand, the discriminant analysis classification model was able to classify the FPO and AO into two distinct groups. Improvement of the principles of combined techniques in authenticating AO from fresh oil is beneficial as a guideline to detect adulteration in cooking oil.

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Aims: Aflatoxin B 1 (AFB 1 ) is considered as the most toxic food contaminant, and microorganisms, especially bacteria, have been studied for their potential to reduce the bioavailability of mycotoxins including aflatoxins. Therefore, this research investigated the efficacy of oral administration of Lactobacillus casei Shirota (LcS) in aflatoxin-induced rats. Methods and Results: Sprague Dawley rats were divided into three groups of untreated control, the group induced with AFB 1 only, and the group given probiotic in addition to AFB 1 . In the group induced with AFB 1 only, food intake and body weight were reduced significantly. The liver and kidney enzymes were significantly enhanced in both groups induced with AFB 1 , but they were lower in the group given LcS. AFB 1 was detected from all serum samples except for untreated control group's samples. Blood serum level of AFB 1 in the group induced with AFB 1 only was significantly higher than the group which received probiotic as a treatment (P < 0Á05), and there was no significant difference between the control group and the group treated with probiotic. Conclusions: LcS supplementation could improve the adverse effect of AFB 1 induction on rats' body weight, plasma biochemical parameters and also could reduce the level of AFB 1 in blood serum. Significance and Impact of the Study: This study's outcomes contribute to better understanding of the potential of probiotic to reduce the bioavailability ofAFB 1 . Moreover, it can open an opportunity for future investigations to study the efficacy of oral supplementation of probiotic LcS in reducing aflatoxin level in human.

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Tocotrienol-rich fraction (TRF) is an extract of palm oil that consists of 25% α-tocopherol and 75% tocotrienols. TRF was shown to possess antioxidant, anti-inflammatory, anticancer, neuroprotective and cholesterol-lowering activities. Glutamate is the major mediator of excitatory signals in the mammalian central nervous system. Extreme amounts of glutamate in the extracellular spaces can lead to numerous neurodegenerative diseases. Hence, the efficacy of oil palm TRF and α-tocopherol in protecting astrocytes against glutamate-induced cell death was studied. Specifically, the effectiveness of pre-or post-treatment of TRF and αtocopherol upon glutamate excitotoxicity was determined by evaluating cell viability and morphology of astrocytes. Cell viability was measured using MTT assay while cell morphology was monitored under fluorescent microscope using the acridine orange/propidium iodide (AO/PI) assay. Exposure to 230 mM glutamate significantly reduced cell viability to 50% in both the pre-and post-treatment studies; however, pre-and post-treatment with TRF and α-tocopherol attenuated the cytotoxic effect of glutamate. Compared to glutamate-injured astrocytes, pre-treatment with 100, 200 and 300 ng/ml TRF significantly improved cell viability following glutamate injury to 86.6%, 86.7% and 93.9%, respectively (p < 0.05). On the contrary, high concentrations of α-tocopherol promote cell death. This study shows that TRF not only provide a better protection against glutamate toxicity (pre-treatment), but was also able to reverse the lipid peroxidation resulting from glutamate insults (post-treatment). The present results demonstrate that TRF, but not αtocopherol, protected the astrocytes against glutamate-induced cell death, indicating its neuro-protective potential.

Summary:In view of the high anti-oxidative potential of tocotrienol, the role of the tocotrienol-rich fraction (TRF) of palm oil in preventing pregnancy induced hypertension (PIH) was explored in a randomized double-blind placebo-controlled clinical trial in an urban teaching hospital. Healthy primigravidae were randomized to receive either oral TRF 100mg daily or placebo, from early second trimester until delivery. Out of 299 women, 151 were randomized into the TRF arm and 148 into the placebo arm. A total of 15 (5.0%) developed PIH. Although there was no statistically significant difference in the incidence of PIH (4/151 or 2.6% in the TRF arm vs 11/148 or 7.4% in the placebo arm, p = 0.058) between the two arms, there was a tendency towards a lower incidence of PIH in the TRF arm compared to the placebo arm. With TRF supplementation, the relative risk (RR) of PIH was 0.36 (95% CI 0.12-1.09). In conclusion, although TRF from palm oil does not statistically significantly reduce the risk of development of PIH in the population studied, the 64% reduction in incidence of PIH is substantial. The findings warrant further clinical trials, particularly in high risk populations.

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