Cardioprotective effect of virgin coconut oil in heated palm oil diet-induced hypertensive rats.

CONTEXT: Virgin coconut oil (VCO) contains high antioxidant activity which may have protective effects on the heart in hypertensive rats. OBJECTIVES: The study investigated the effects of VCO on blood pressure and cardiac tissue by measuring angiotensin-converting enzyme (ACE) activity and its histomorphometry in rats fed with a heated palm oil (HPO) diet. MATERIALS AND METHODS: Thirty-two male Sprague-Dawley rats were randomly divided into four groups: (i) control, (ii) orally given VCO (1.42 ml/kg), (iii) fed with a HPO (15%) diet, and (iv) fed with a HPO diet and supplemented with VCO (1.42 ml/kg, po) (HPO+VCO) for 16 weeks. Blood pressure was measured monthly. After 16 weeks, rat hearts were dissected for lipid peroxidation (TBARS) and ACE activity measurement and histomorphometric study. RESULTS: Systolic blood pressure was significantly increased in the HPO group compared with the control starting at week eight (112.91 ± 1.32 versus 98.08 ± 3.61 mmHg, p < 0.05) which was prevented by VCO supplementation (91.73 ± 3.42 mmHg). The consumption of HPO increased TBARS and ACE activity in heart, which were inhibited by VCO supplementation. The increases in the myofiber width and area as well as nuclear size reduction in the HPO group were significantly prevented by VCO supplementation. CONCLUSION: These results suggested that VCO supplementation possesses a cardioprotective effect by preventing the increase in blood pressure via an antioxidant mechanism and remodeling in rats fed repeatedly with a HPO diet.

The role of repeatedly heated soybean oil in the development of hypertension in rats: association with vascular inflammation.

Thermally oxidized oil generates reactive oxygen species that have been implicated in several pathological processes including hypertension. This study was to ascertain the role of inflammation in the blood pressure raising effect of heated soybean oil in rats. Male Sprague-Dawley rats were divided into four groups and were fed with the following diets, respectively, for 6 months: basal diet (control); fresh soybean oil (FSO); five-time-heated soybean oil (5HSO); or 10-time-heated soybean oil (10HSO). Blood pressure was measured at baseline and monthly using tail-cuff method. Plasma prostacyclin (PGI(2) ) and thromboxane A(2) (TXA(2) ) were measured prior to treatment and at the end of the study. After six months, the rats were sacrificed, and the aortic arches were dissected for morphometric and immunohistochemical analyses. Blood pressure was increased significantly in the 5HSO and 10HSO groups. The blood pressure was maintained throughout the study in rats fed FSO. The aortae in the 5HSO and 10HSO groups showed significantly increased aortic wall thickness, area and circumferential wall tension. 5HSO and 10HSO diets significantly increased plasma TXA(2) /PGI(2) ratio. Endothelial VCAM-1 and ICAM-1 were significantly increased in 5HSO, as well as LOX-1 in 10HSO groups. In conclusion, prolonged consumption of repeatedly heated soybean oil causes blood pressure elevation, which may be attributed to inflammation.

Calcaneal quantitative ultrasound value for middle-aged and elderly Malaysian Chinese men and its association with age and body anthropometry.

Quantitative ultrasound (QUS) is a relatively easy, reliable, and safe method for bone status assessment, but reference data for Asian males remain scarce. Our study aimed to determine the values for one QUS parameter, the speed of sound (SOS) at the calcaneus, in Malaysian Chinese men and to determine the association between the SOS and several demographic characteristics, such as age, weight, height, and body mass index. Three hundred forty-eight Malaysian Chinese men aged 40 yr and older were recruited, and their calcaneal QUS value was determined using the CM-200 densitometer (Furuno Electric, Nishinomiya City, Japan). The results indicated a significant correlation between SOS and age, and multiple stepwise regression analysis indicated that age and height were important predictors of SOS. A significant reduction in SOS value was observed when men 60 yr and older were compared with men aged 40-49 yr. Compared with the reference data for Japanese males, Chinese men in Malaysia showed higher SOS values across all the age groups studied. In conclusion, there is an age-related decrease in SOS values in Malaysian Chinese men, and the SOS values established in this study can be used as a reference for future studies.

Beneficial effects of tocotrienol and tocopherol on bone histomorphometric parameters in sprague-dawley male rats after nicotine cessation.

This study was conducted to determine the effectiveness of three forms of vitamin E supplements following nicotine treatment on bone histomorphometric parameters in an adult male rat model. Rats were divided into seven groups: baseline (B, killed without treatment), control (C, normal saline for 4 months), nicotine (N, nicotine for 2 months), nicotine cessation (NC), tocotrienol-enhanced fraction (TEF), gamma-tocotrienol (GTT), and alpha-tocopherol (ATF). Treatments for the NC, TEF, GTT, and ATF groups were performed in two phases. For the first 2 months they were given nicotine (7 mg/kg), and for the following 2 months nicotine administration was stopped and treatments with respective vitamin E preparations (60 mg/kg) were commenced except for the NC group, which was allowed to recover without treatment. Rats in the N and NC groups had lower trabecular bone volume, mineral appositional rate (MAR), and bone formation rate (BFR/BS) and higher single labeled surface and osteoclast surface compared to the C group. Vitamin E treatment reversed these nicotine effects. Both the TEF and GTT groups, but not the ATF group, had a significantly higher trabecular thickness but lower eroded surface (ES/BS) than the C group. The tocotrienol-treated groups had lower ES/BS than the ATF group. The GTT group showed a significantly higher MAR and BFR/BS than the TEF and ATF groups. In conclusion, nicotine induced significant bone loss, while vitamin E supplements not only reversed the effects but also stimulated bone formation significantly above baseline values. Tocotrienol was shown to be slightly superior compared to tocopherol. Thus, vitamin E, especially GTT, may have therapeutic potential to repair bone damage caused by chronic smoking.

Palm tocotrienol-rich fraction inhibits methionine-induced cystathionine ß-synthase in rat liver.

Oxidative stress plays an important role in cardiovascular diseases. The study investigated the effects of dietary palm tocotrienol-rich fraction on homocysteine metabolism in rats fed a high-methionine diet. Forty-two male Wistar rats were randomly assigned to six groups. Five groups were fed with high-methionine diet (1%) for 10 weeks. Groups 2 to 5 were also given dietary folate (8 mg/kg) and three doses of palm tocotrienol-rich fraction (30, 60 and 150 mg/kg) from week 6 to week 10. The last group was only given basal rat chow. High-methionine diet increased plasma homocysteine after 10 weeks, which was prevented by the supplementations of folate and high-dose palm tocotrienol-rich fraction. Hepatic S-adenosyl methionine (SAM) content was unaffected in all groups but S-adenosyl homocysteine (SAH) content was reduced in the folate group. Folate supplementation increased the SAM/SAH ratio, while in the palm tocotrienol-rich fraction groups, the ratio was lower compared with the folate. Augmented activity of hepatic cystathionine ß-synthase and lipid peroxidation content by high-methionine diet was inhibited by palm tocotrienol-rich fraction supplementations (moderate and high doses), but not by folate. The supplemented groups had lower hepatic lipid peroxidation than the high-methionine diet. In conclusion, palm tocotrienol-rich fraction reduced high-methionine-induced hyperhomocysteinaemia possibly by reducing hepatic oxidative stress in high-methionine-fed rats. It may also exert a direct inhibitory effect on hepatic cystathionine ß-synthase.

Palm tocotrienol-rich fraction improves vascular proatherosclerotic changes in hyperhomocysteinemic rats.

This study investigated the effects of palm tocotrienol-rich fraction (TRF) on aortic proatherosclerotic changes in rats fed with a high methionine diet. Forty-two male Wistar rats were divided into six groups. The first group was the control (fed with a basal diet). Another five groups were fed with 1% methionine diet for 10 weeks. From week 6 onward, folate (8 mg/kg diet) or palm TRF (30, 60, and 150 mg/kg diets) was added into the diet of the last four rat groups, respectively. The high methionine diet raised the plasma total homocysteine and aortic lipid peroxidation, which were reduced by the palm TRF and folate supplementations. Plasma nitric oxide was reduced in the high methionine group compared to the control (3.72 ± 0.57 versus 6.65 ± 0.53 µ mol/L, P < 0.05), which reduction was reversed by the palm TRF (60 and 150 mg/kg) and folate supplementations. The increased aortic vascular cell adhesion molecule-1 expression in the methionine group (2.58 ± 0.29) was significantly reduced by the folate (1.38 ± 0.18) and palm TRF at 150 mg/kg (1.19 ± 0.23). Palm TRF was comparable to folate in reducing high methionine diet-induced plasma hyperhomocysteinemia, aortic oxidative stress, and inflammatory changes in rats.

Palm tocotrienol-rich fraction reduced plasma homocysteine and heart oxidative stress in rats fed with a high-methionine diet.

Oxidative stress contributes to cardiovascular diseases. We aimed to study the effects of palm tocotrienol-rich fraction (TRF) on plasma homocysteine and cardiac oxidative stress in rats fed with a high-methionine diet. Forty-two male Wistar rats were divided into six groups. The first group was the control. Groups 2-6 were fed 1% methionine diet for 10 weeks. From week 6 onward, folate (8 mg/kg diet) or palm TRF (30, 60 and 150 mg/kg diet) was added into the diet of groups 3, 4, 5 and 6. The rats were then killed. Palm TRF at 150 mg/kg and folate supplementation prevented the increase in plasma total homocysteine (4.14 ± 0.33 and 4.30 ± 0.26 vs 5.49 ± 0.25 mmol/L, p < 0.05) induced by a high-methionine diet. The increased heart thiobarbituric acid reactive substance in rats fed with high-methionine diet was also prevented by the supplementations of palm TRF (60 and 150 mg/kg) and folate. The high-methionine group had a lower glutathione peroxidase activity (49 ± 3 vs 69 ± 4 pmol/mg protein/min) than the control group. This reduction was reversed by palm TRF at 60 and 150 mg/kg diet (p < 0.05), but not by folate. Catalase and superoxide dismutase activities were unaffected by both methionine and vitamin supplementations. In conclusion, palm TRF was comparable to folate in reducing high-methionine diet-induced hyperhomocysteinemia and oxidative stress in the rats' hearts. However, palm TRF was more effective than folate in preserving the heart glutathione peroxidase enzyme activity.

Involvement of inflammation and adverse vascular remodelling in the blood pressure raising effect of repeatedly heated palm oil in rats.

Oil thermoxidation during deep frying generates harmful oxidative free radicals that induce inflammation and increase the risk of hypertension. This study aimed to investigate the effect of repeatedly heated palm oil on blood pressure, aortic morphometry, and vascular cell adhesion molecule-1 (VCAM-1) expression in rats. Male Sprague-Dawley rats were divided into five groups: control, fresh palm oil (FPO), one-time-heated palm oil (1HPO), five-time-heated palm oil (5HPO), or ten-time-heated palm oil (10HPO). Feeding duration was six months. Blood pressure was measured at baseline and monthly using tail-cuff method. After six months, the rats were sacrificed and the aortic arches were dissected for morphometric and immunohistochemical analyses. FPO group showed significantly lower blood pressure than all other groups. Blood pressure was increased significantly in 5HPO and 10HPO groups. The aortae of 5HPO and 10HPO groups showed significantly increased thickness and area of intima-media, circumferential wall tension, and VCAM-1 than other groups. Elastic lamellae were disorganised and fragmented in 5HPO- and 10HPO-treated rats. VCAM-1 expression showed a significant positive correlation with blood pressure. In conclusion, prolonged consumption of repeatedly heated palm oil causes blood pressure elevation, adverse remodelling, and increased VCAM-1, which suggests a possible involvement of inflammation.

Vitamin E reversed nicotine-induced toxic effects on bone biochemical markers in male rats.

INTRODUCTION: Vitamin E is beneficial in restoring bone histomorphometric parameters in nicotine-treated rats. This study determined the effectiveness of 3 forms of vitamin E in restoring bone metabolism in nicotine-treated rats. MATERIAL AND METHODS: Thirty-five male Sprague-Dawley rats were divided into 5 groups: (1) control (C), (2) nicotine cessation (NC), (3) α-tocopherol (ATF), (4) tocotrienol-enhanced fraction (TEF) and (5) γ-tocotrienol (GTT). Treatment was carried out for 4 months. The control group was administered normal saline and olive oil throughout the treatment period while treatment for groups 2-5 was performed in 2 phases. In the first phase, the groups received nicotine 7 mg/kg intraperitoneally for 2 months. The following 2 months, group 2 received normal saline and olive oil while groups 3-5 received ATF, TEF or GTT, 60 mg/kg orally. Pre-treatment and post-treatment serum was collected for bone biochemical marker measurement using the ELISA method. RESULTS: Nicotine increased serum bone-resorbing cytokines (interleukin-1 and interleukin-6) and the bone resorption marker pyridinoline (PYD) while reducing the bone formation marker osteocalcin after 2 months of nicotine treatment. The parameters failed to improve after nicotine was stopped for 2 months. Supplementation with the 3 forms of vitamin E improved the parameters, i.e. reduced the cytokines and pyridinoline as well as increased the osteocalcin. In addition, the TEF and GTT groups had a higher level of osteocalcin than the control group. CONCLUSIONS: Nicotine impaired bone metabolism and cessation of nicotine treatment did not reverse the effects. Vitamin E, especially the tocotrienols, restored bone metabolism that was impaired due to nicotine.