Utilization of plant extracts to control the safety and quality of fried foods-A review.

Frying is one of the most common methods of preparing foods. However, it may lead to the formation of potentially hazardous substances, such as acrylamide, heterocyclic amines, trans fatty acids, advanced glycation end products, hydroxymethyl furfural and polycyclic aromatic hydrocarbons, and adversely alter the desirable sensory attributes of foods, thereby reducing the safety and quality of fried foods. Currently, the formation of toxic substances is usually reduced by pretreatment of the raw materials, optimization of process parameters, and the use of coatings. However, many of these strategies are not highly effective at inhibiting the formation of these undesirable reaction products. Plant extracts can be used for this purpose because of their abundance, safety, and beneficial functional attributes. In this article, we focus on the potential of using plant extracts to inhibit the formation of hazardous substances, so as to improve the safety of fried food. In addition, we also summarized the effects of plant extracts, which inhibit the production of hazardous substances, on food sensory aspects (flavor, color, texture, and taste). Finally, we highlight areas where further research is required.

Optimization and validation of in-situ derivatization and headspace solid-phase microextraction for gas chromatography-mass spectrometry analysis of 3-MCPD esters, 2-MCPD esters and glycidyl esters in edible oils via central composite design.

This study aimed to develop a headspace solid-phase microextraction gas chromatography-mass spectrometry (HS-SPME-GC-MS) method for the quantification of 3-monochloropropane-1,2-diol fatty acid esters (3-MCPDEs) and 2-monochloropropane-1,3-diol fatty acid esters (2-MCPDEs), and semi-quantification of glycidyl fatty acid esters (GEs) in edible oils. A central composite design was implemented to optimize the derivatization temperature and extraction time, which were 100 °C and 80 min, respectively. HS-SPME coupled with in-situ derivatization was more straightforward (three steps) and sensitive, with a limit of detection of 16% (3.9 µg/L) and 11% (5.3 µg/L) higher than that of liquid injection method, for 3-MCPD and 2-MCPD, respectively. The recoveries of 3-MCPD and 2-MCPD were in the range of 91.1% to 102.1%, with a relative standard deviation ranging from 0.08 to 9.29%. The validated methodology was successfully applied to oil samples. Further efforts will focus on shortening the extraction time, as 80 min is relatively long.

Knockdown of delta-5-desaturase promotes the anti-cancer activity of dihomo-γ-linolenic acid and enhances the efficacy of chemotherapy in colon cancer cells expressing COX-2.

Cyclooxygenase (COX), commonly overexpressed in cancer cells, is a major lipid peroxidizing enzyme that metabolizes polyunsaturated fatty acids (ω-3s and ω-6s). The COX-catalyzed free radical peroxidation of arachidonic acid (ω-6) can produce deleterious metabolites (e.g. 2-series prostaglandins) that are implicated in cancer development. Thus, COX inhibition has been intensively investigated as a complementary therapeutic strategy for cancer. However, our previous study has demonstrated that a free radical-derived byproduct (8-hydroxyoctanoic acid) formed from COX-catalyzed peroxidation of dihomo-γ-linolenic acid (DGLA, the precursor of arachidonic acid) can inhibit colon cancer cell growth. We thus hypothesize that the commonly overexpressed COX in cancer (~90% of colon cancer patients) can be taken advantage to suppress cell growth by knocking down delta-5-desaturase (D5D, a key enzyme that converts DGLA to arachidonic acid). In addition, D5D knockdown along with DGLA supplement may enhance the efficacy of chemotherapeutic drugs. After knocking down D5D in HCA-7 colony 29 cells and HT-29 cells (human colon cancer cell lines with high and low COX levels, respectively), the antitumor activity of DGLA was significantly enhanced along with the formation of a threshold range (~0.5-1.0µM) of 8-hydroxyoctanoic acid. In contrast, DGLA treatment did not inhibit cell growth when D5D was not knocked down and only limited amount of 8-hydroxyoctanoic acid was formed. D5D knockdown along with DGLA treatment also enhanced the cytotoxicities of various chemotherapeutic drugs, including 5-fluorouracil, regorafenib, and irinotecan, potentially through the activation of pro-apoptotic proteins, e.g. p53 and caspase 9. For the first time, we have demonstrated that the overexpressed COX in cancer cells can be utilized in suppressing cancer cell growth. This finding may provide a new option besides COX inhibition to optimize cancer therapy. The outcome of this translational research will guide us to develop a novel ω-6-based diet-care strategy in combination with current chemotherapy for colon cancer prevention and treatment.