Level of knowledge, attitude and practice of night market food outlet operators in Kuala Lumpur regarding the usage of repeatedly heated cooking oil.

Consumption of repeatedly heated oil can be detrimental to health. The objective of this study was to determine the level of knowledge, attitude and practice of night market food outlet operators in Kuala Lumpur regarding the usage of repeatedly heated cooking oil. The quality of cooking oil was also investigated. A cross-sectional study involving pretested questionnaire was undertaken in April 2009. The questionnaire was designed as a tool to collect data from the respondents (n=100) by face-to-face interview. The results showed that majority of respondents had only moderate (53.0%) or low (18.0%) level of knowledge regarding this issue. Most respondents (67.0%) agreed that it is not a good practice. The majority (69.0%) agreed that the usage of repeatedly heated cooking oil is detrimental to health. Despite that, most respondents (63.0%) admitted that they had used cooking oil repeatedly. Most (62.0%) of the cooking oil samples taken from the night market food outlets were considered fit for human consumption. In conclusion, the level of knowledge of night market food outlet operators in Kuala Lumpur regarding this issue needs to be improved in order to ensure the safety of fried food purchased from such establishments.

Enzymatic and microstructural changes in the liver of experimental rats fed with fatty diet and fresh or heated soy oil concurrently.

AIMS: Consumption of heated edible oils may be harmful. The present study aimed to observe the histological changes due to concurrent consumption of soy oil (either fresh or heated) and fatty diet and the changes in the level of alanine transaminase (ALT) and alkaline phosphatase (ALP). MATERIALS AND METHODS: Forty female Spraque-Dawley rats were equally divided into four groups (I to IV). All the rats n groups II, III and IV were ovariectomised. Rats in group I (control) were fed with 2% cholesterol diet, whereas the rats in groups II, III and IV were fed with 2% cholesterol diet fortified with 15% weight/weight (w/w) fresh soy oil (FSO), once heated soy oil (1HSO) and five times heated soy oil (5HSO) respectively, for 16 weeks. Blood was taken for liver enzymes and analysed before and after 16 weeks of study. At the end of the study the animals were sacrificed, and the liver was examined histologically. The specimens were weighed, formalin fixed and the sections were stained with hematoxylin and eosin. RESULTS: Fresh, 1HSO and 5HSO soy oil caused significant increase in serum ALT and ALP compared to their base line values. Fresh, 1HSO and 5HSO soy oil caused microsteatosis, inflammation and necrosis of the liver tissues. However, there was no significant difference in the ALT and ALP enzyme levels amongst the oil fed groups. CONCLUSION: It is concluded that the effect of both fresh and heated soy oil on these parameters was not affected by repeated heating except for the inflammation.

Effect of palm vitamin E on the healing of ethanol-induced gastric injury in rats.

The effect of palm vitamin E on the healing of ethanol-induced gastric lesions and various biochemical parameters were investigated. The study was divided into two phases. In the first phase of the study, 42 rats of Sprague Dawley species (200-250 gm weight) were randomly divided into two groups fed with a normal diet (control) or palm vitamin E enriched diet (150 mg/kg) for 3 weeks. The rats were killed after 3 weeks of feeding. Gastric tissue contents of malondialdehyde (MDA), prostaglandin E2 and acid were measured. In the second phase of the study 42 rats were divided into two groups. Group 1 was fed normal rat pellets (control) and group 2 was fed palm vitamin E enriched pellets (150 mg/kg food) for 3 weeks. After 3 weeks of feeding gastric mucosal injury was induced by an orogastric tube administration of 0.5 ml 100% ethanol. The rats were killed at 1 hour, 4 hours and 1 week after ethanol exposure for semiquantitative determination of ulcer index and gastric acid concentration. Gastric tissue MDA and mucus were measured only at 1 week after ethanol exposure. In the first phase of the study we found that palm vitamin E only caused a significant reduction in gastric MDA. However, it showed no significant effects on prostaglandin E2 and gastric acid concentration. In the second phase of the study, the mean ulcer index of palm vitamin E supplemented group killed after 1 week of ethanol exposure was significantly lower compared to the respective control. However, there was no significant difference in ulcer index in rats killed at 1 hour and 24 hours after ethanol exposure. The gastric acid concentration was significantly higher in the group treated with palm vitamin E killed 1 week after ethanol exposure compared to control. The gastric tissue MDA was significantly lower in the palm vitamin E supplemented group compared to control. There was no significant difference in gastric mucus content of the both groups. The ulcer healing which occurred in the presence of a high gastric acid suggests that the effect of palm vitamin E on the healing of gastric lesions was not mediated via a reduction in gastric acid nor was it mediated through increasing prostaglandin E2 or mucus production. The most probable mechanism is via reducing lipid peroxidation as reflected by a significant decreased in gastric tissue MDA content.

Vitamin E and factors affecting atherosclerosis in rabbits fed a cholesterol-rich diet.

The present study aims to examine the effects of a palm-oil-derived vitamin E mixture containing tocotrienol (approximately 70%) and tocopherol (approximately 30%) on plasma lipids and on the formation of atherosclerotic plaques in rabbits given a 2% cholesterol diet. Eighteen New Zealand White rabbits (2.2-2.8 kg) were divided into three groups; group 1 (control) was fed a normal diet, group 2 (AT) was fed a 2% cholesterol diet and group 3 (PV) was fed a 2% cholesterol diet with oral palm vitamin E (60 mg/kg body weight) given daily for 10 weeks. There were no differences in the total cholesterol and triacylglycerol levels between the AT and PV groups. The PV group had a significantly higher concentrations of HDL-c and a lower TC/HDL-c ratio compared to the AT group (P < 0.003). The aortic tissue content of cholesterol and atherosclerotic lesions were comparable in both the AT and PV groups. However, the PV group had a lower content of plasma and aortic tissue malondialdehyde (P < 0.005). Our findings suggest that despite a highly atherogenic diet, palm vitamin E improved some important plasma lipid parameters, reduced lipid peroxidation but did not have an effect on the atherosclerotic plaque formation.

Comparative effect of palm vitamin E and ranitidine on the healing of ethanol-induced gastric lesions in rats.

The effect of palm vitamin E on the healing of ethanol-induced gastric lesion was compared with ranitidine. Fifty-six male rats of Sprague-Dawley species (200-250 g of weight) were randomly divided into three groups (N = 14). Gastric mucosal injury was induced by orogastric tube administration of 0.5 ml 100% ethanol. Immediately after induction, Group I (k) rats was fed with a normal diet (control), group II (p) was fed palm vitamin E enriched diet (150 mg/kg food), Group III(r) was treated with ranitidine 30 mg/kg body weight intraperitoneally and Group IV (p + r) was fed with palm vitamin E and treated with ranitidine 30 mg/kg body weight intraperitoneally of the same dose. The rats were killed at the end of 1 week and 3 weeks of treatment or feeding. The rate of gastric healing was faster in palm vitamin E treated group compared to control and ranitidine treated groups as shown by a lower mean ulcer index. The effect was seen as early as the first week of treatment whereas ranitidine did not show any healing effect even after 3 weeks of therapy. Neither gastric acidity nor gastric mucus production are involved in gastroprotective effect of palm vitamin E. The most probable mechanism is via reducing lipid peroxidation process as shown by a significant decrease in gastric MDA.

Palm vitamin E and the healing of ethanol-induced gastric lesions.

The main focus of the study was to examine the effect of palm vitamin E (a tocotrienol-enriched fraction of palm oil) on the healing of ethanol-induced gastric mucosal lesions. The study was divided into three sections.Study 1 determined the gastric content of vitamin E after dietary supplementation with palm vitamin E for 3 weeks. Seven rats were fed a normal diet and another 7 were fed a palm vitamin E-enriched diet (150 mg/kg food). The gastric content of vitamin E levels were higher in rats fed with a palm vitamin E-enriched diet (p<0.01). Study 2 determined the time-dependent effects of palm vitamin E on gastric lesions and gastric acidity postethanol administration. Two groups of rats were fed either a normal rat diet or a palm vitamin E-enriched diet (150 mg/kg food). After 3 weeks, the control and a treated group received a single intragastric dose of 100% ethanol. Assessment of gastric lesions after 1 week showed a lower gastric lesion index in the palm vitamin E group compared with the controls (p<0.05) but there was no difference in the gastric acid content after 1 week between the two groups. Study 3 determined the effects of palm vitamin E on the gastric tissue content of malondialdehyde (MDA), PGE2 and gastric acidity without ethanol administration. The MDA content was lower in the palm vitamin E-treated group (p<0.05). However, the gastric acid and PGE2 content in both groups did not differ. The findings suggest that feeding with a palm vitamin E-enriched diet (150 mg/kg food) for 3 weeks resulted in a significant concentration of vitamin E in the gastric tissue. It was concluded that palm vitamin E may promote the healing of ethanol-induced gastric lesions through minimizing the lipid preoccupation process in the gastric mucous.

Effects of nicardipine on lipid peroxidation in rabbits given 2% cholesterol diet.

Nicardipine has been shown to have an anti-atherogenic effect in rabbits given a 2% cholesterol diet. Current evidence suggests that lipid peroxidation plays an important role in atherogenesis. This study examines the effect of nicardipine on lipid peroxidation in rabbits given a 2% cholesterol diet, 8 of these rabbits given nicardipine 0.5 mg/kg twice daily intramuscularly for ten weeks while the remaining untreated 6 were controls. After ten weeks, serum malondialdehyde in the control group was significantly higher compared to their baseline levels (P < 0.05). However, there was no increase in serum malondialdehyde in the nicardipine group after 10 weeks. The area of Sudan IV positive intimal lesions (atherosclerotic plaques) were significantly decreased (P < 0.01) in the treated group compared to the control group. The aortic tissue content of cholesterol and diene conjugates were also decreased in the nicardipine group (P < 0.01). These findings suggest a possible link between nicardipine and lipid peroxidation in mediating its antiatherogenic effects.

Influence of dietary fat on plasma lipid profiles of Malaysian adolescents.

We studied the effects of saturated (palm olein) and polyunsaturated (soybean oil) cooking oils on the lipid profiles of Malaysian male adolescents eating normal Malaysian diets for 5 wk. Diets cooked with palm olein did not significantly alter plasma total-cholesterol, LDL cholesterol, and HDL cholesterol concentrations or the ratio of total cholesterol to HDL cholesterol compared with diets cooked with soybean oil. However, the diet cooked with palm olein significantly increased apolipoprotein A-I (11%) and apolipoprotein B (9%) concentrations. Unexpectedly, soybean-oil-cooked diets caused a significant increase (47%) in plasma triglycerides compared with palm-olein-cooked diets. We conclude that palm olein, when used as cooking oil, has no detrimental effects on plasma lipid profiles in Malaysian adolescents.