Objective:The frequent consumption of deep-fried foods has been linked to high risk of certain non-communicable diseases.As a consequence,the safety of deep-fried oil(DFO)ingested with fried foods has been called into...Objective:The frequent consumption of deep-fried foods has been linked to high risk of certain non-communicable diseases.As a consequence,the safety of deep-fried oil(DFO)ingested with fried foods has been called into question.This study therefore evaluated the effects of DFO from palm kernel on serum 4-hydroxynonenal protein adduct formation,De Ritis ratio(DRR),liver histology and atherogenicity in Wistar rats and the role of vitamin C intervention.Methods:Deep-fried oil samples were characterized for total antioxidant capacity(TAC),degradation and metal contamination levels and compared against counterpart unused frying oil(UFO).In the animal experiment,both oil samples,sourced from commercial cooks,were orally administered,for 13 weeks,to sixty-two rats randomly divided into six test groups of two exposure levels alongside vitamin C control.After exposure,serum liver enzyme activities and lipoproteins levels were determined using colorimetric methods,while protein adducts levels were determined using enzyme-linked immunosorbent assay(ELISA).Histopathological examinations of liver tissues were also performed.Results:DFO had significantly lower(P=0.021)TAC,significantly higher(P=0.024)volatile acid and Pb concentrations compared to UFO.Exposure to DFO significantly increased(P<0.01)serum protein adduct formation,the De Ritis ratio and caused cytoplasmic vacuolation and pigment deposit on liver tissues compared to the control.Additionally,DFO exposures had an initial negative body weight gain rate that increased at the end of the study.Conclusion:However,co-administration of vitamin C significantly reduced(P<0.05)the De Ritis ratio and reduced the serum protein adducts levels by at least 15%.Concomitant intake of vitamin C and DFO can mitigate probable adverse effects.展开更多
The lipid oxidation product, the toxic 4-hydroxynonenal, was measured for fried chicken in commercial samples from two fast food restaurants and one commercial establishment. The fried chicken samples were breasts, th...The lipid oxidation product, the toxic 4-hydroxynonenal, was measured for fried chicken in commercial samples from two fast food restaurants and one commercial establishment. The fried chicken samples were breasts, thighs, chicken nuggets and popcorn chicken. Fried chicken samples were separated to breast skin and meat, and thigh skin and meat. Chicken nuggets and popcorn chicken were not separated from the coating materials and the meat was analyzed together. Samples were analyzed for total fat, fatty acid distribution, reactivity with thiobarbituric acid (TBAR), measuring the secondary lipid peroxidation products such as aldehydes, ketones and related carbonyl compounds. Samples were analyzed for HNE, a toxic aldehyde using high performance liquid chromatography (HPLC). Fatty acid distribution showed in breast and thigh meats, a higher level of palmitic acid, compared to the breast and thigh skins. TBAR values were significantly higher in all breast meats compared to skins. TBAR values were significantly higher in thigh meat than in skin samples. HNE concentrations (μg HNE/g fat) were significantly very low in breast skins compared to breast meat. HNE concentration was generally higher in thigh meat than skin but not in every sample. In chicken nuggets, both the TBAR value and HNE concentration were much higher from one establishment than from the two others. Chicken nuggets TBAR and HNE concentrations resembled one of the chicken nugget samples. The average toxic HNE concentration for 100 g fried chicken breast (skins + meat) was 12.55 μg and for thighs (skin + meat) was 26.76 μg. The average total HNE concentration was 2.1 times higher in the fried chicken thighs than in the breasts. It is clear that HNE is produced during the heating process of oils and incorporated into the fried meat and skin samples during the frying process. If HNE, a toxic aldehyde, is consumed with the food, over long periods of time it could be related to a number of pathological conditions.展开更多
文摘Objective:The frequent consumption of deep-fried foods has been linked to high risk of certain non-communicable diseases.As a consequence,the safety of deep-fried oil(DFO)ingested with fried foods has been called into question.This study therefore evaluated the effects of DFO from palm kernel on serum 4-hydroxynonenal protein adduct formation,De Ritis ratio(DRR),liver histology and atherogenicity in Wistar rats and the role of vitamin C intervention.Methods:Deep-fried oil samples were characterized for total antioxidant capacity(TAC),degradation and metal contamination levels and compared against counterpart unused frying oil(UFO).In the animal experiment,both oil samples,sourced from commercial cooks,were orally administered,for 13 weeks,to sixty-two rats randomly divided into six test groups of two exposure levels alongside vitamin C control.After exposure,serum liver enzyme activities and lipoproteins levels were determined using colorimetric methods,while protein adducts levels were determined using enzyme-linked immunosorbent assay(ELISA).Histopathological examinations of liver tissues were also performed.Results:DFO had significantly lower(P=0.021)TAC,significantly higher(P=0.024)volatile acid and Pb concentrations compared to UFO.Exposure to DFO significantly increased(P<0.01)serum protein adduct formation,the De Ritis ratio and caused cytoplasmic vacuolation and pigment deposit on liver tissues compared to the control.Additionally,DFO exposures had an initial negative body weight gain rate that increased at the end of the study.Conclusion:However,co-administration of vitamin C significantly reduced(P<0.05)the De Ritis ratio and reduced the serum protein adducts levels by at least 15%.Concomitant intake of vitamin C and DFO can mitigate probable adverse effects.
文摘The lipid oxidation product, the toxic 4-hydroxynonenal, was measured for fried chicken in commercial samples from two fast food restaurants and one commercial establishment. The fried chicken samples were breasts, thighs, chicken nuggets and popcorn chicken. Fried chicken samples were separated to breast skin and meat, and thigh skin and meat. Chicken nuggets and popcorn chicken were not separated from the coating materials and the meat was analyzed together. Samples were analyzed for total fat, fatty acid distribution, reactivity with thiobarbituric acid (TBAR), measuring the secondary lipid peroxidation products such as aldehydes, ketones and related carbonyl compounds. Samples were analyzed for HNE, a toxic aldehyde using high performance liquid chromatography (HPLC). Fatty acid distribution showed in breast and thigh meats, a higher level of palmitic acid, compared to the breast and thigh skins. TBAR values were significantly higher in all breast meats compared to skins. TBAR values were significantly higher in thigh meat than in skin samples. HNE concentrations (μg HNE/g fat) were significantly very low in breast skins compared to breast meat. HNE concentration was generally higher in thigh meat than skin but not in every sample. In chicken nuggets, both the TBAR value and HNE concentration were much higher from one establishment than from the two others. Chicken nuggets TBAR and HNE concentrations resembled one of the chicken nugget samples. The average toxic HNE concentration for 100 g fried chicken breast (skins + meat) was 12.55 μg and for thighs (skin + meat) was 26.76 μg. The average total HNE concentration was 2.1 times higher in the fried chicken thighs than in the breasts. It is clear that HNE is produced during the heating process of oils and incorporated into the fried meat and skin samples during the frying process. If HNE, a toxic aldehyde, is consumed with the food, over long periods of time it could be related to a number of pathological conditions.
