Protection Against Carbon Tetrachloride-Induced Lipid Peroxidation in the Rat by Dietary Vitamin E, Selenium, and Methionine as Measured by Ethane Evolution

1977 ◽  
Vol 107 (4) ◽  
pp. 656-665 ◽  
Author(s):  
Dean G. Hafeman ◽  
William G. Hoekstra
2003 ◽  
Vol 89 (1) ◽  
pp. 19-28 ◽  
Author(s):  
Morio Saito ◽  
Kazuhiro Kubo

In a previous study, we found that the extent of dietary n-3 docosahexaenoic acid (DHA)-stimulated tissue lipid peroxidation was less than expected from the relative peroxidizability index of the total tissue lipids in rats with adequate vitamin E nutritional status. This suppression of lipid peroxidation was especially prominent in the liver. To elucidate whether this phenomenon was unique to DHA, we compared the peroxidation effects of n-3 α-linolenic acid (α-LN) and n-3 eicosapentaeonic acid (EPA) with those of DHA in rats. Either α-LN (8·6 % of total energy), EPA (8·2 %), or DHA (8·0 %) and one of two levels of dietary vitamin E (7·5 and 54 mg/kg diet) were fed to rats for 22 d. Levels of conjugated diene, chemiluminescence emission and thiobarbituric acid (TBA)-reactive substance in the liver, kidney, and testis were determined as indicators of lipid peroxidation. In rats fed the DHA diet deficient in vitamin E (7·5 m/g diet), TBA values in the liver, kidney, and testis correlated well with the tissues' relative peroxidizability indices. In rats fed the α-LN diet with an adequate level of vitamin E (54 m/g diet), a close association between relative peroxidizability indices and lipid peroxide levels was observed in all the tissues analysed. However, in rats fed either the EPA diet or the DHA diet with an adequate level of vitamin E, the extent of lipid peroxidation in each tissue was less than expected from the relative peroxidizability index. This suppression was particularly marked in the liver. We concluded that suppression of lipid peroxidation below the relative peroxidizability index was not unique to DHA, but was also seen with EPA, which has five double bonds, in rats with adequate vitamin E nutritional status, but not with α-LN, which has three double bonds.


2002 ◽  
Vol 72 (2) ◽  
pp. 91-100 ◽  
Author(s):  
Kazim Sahin ◽  
Osman Kucuk ◽  
Nurhan Sahin ◽  
Mustafa Sari

This study was conducted to determine the effects of dietary vitamin C (L-ascorbic acid) and vitamin E (a-tocopherol acetate) on lipid peroxidation status measured as MDA and serum triiodothyronine (T3), thyroxine (T4), thyroid-stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), as well as some other serum metabolite and mineral concentrations of Japanese quails reared under heat stress (34º C). One hundred-eighty 10-day-old Japanese quails were randomly assigned to six treatment groups, three replicates of 10 birds each. Using a 2 × 3 factorial design, the birds received two levels of vitamin C (100 and 200 mg/kg of diet) or three levels of vitamin E (125, 250, or 500 mg/kg of diet). Greater dietary vitamin E and vitamin C resulted in a greater serum T3, T4, and TSH (p=0.001), but lower ACTH (p=0.001) concentrations. Serum concentrations of T4 and TSH increased to a greater extent by increasing dietary vitamin C when greater vitamin E levels were fed (interaction, p=0.001). Serum glucose, urea, triglycerides, and cholesterol concentrations decreased (p=0.001), while protein and albumin concentrations increased (p =0.001) when both dietary vitamin C and vitamin E were increased. Serum activities of SGOT and SGPT were not influenced by dietary vitamin C or vitamin E (p>0.43). However, serum activity of AP increased (p=0.001) by increasing both dietary vitamin C and vitamin E. Increasing both dietary vitamin C and vitamin E caused an increase in serum concentrations of Ca, P, K (p=0.001), Fe, and Zn (p=0.01) but a decrease in serum concentrations of Na (p=0.001) and Cu (p=0.01). Interactions between vitamin C and vitamin E were detected for Ca, P, Na, and K (p =0.001). Greater dietary vitamin C and vitamin E resulted in a greater serum and liver vitamin E, C, and A (p_0.05), but lower MDA (p=0.001) concentrations. Results of the present study conclude that supplementing a combination of dietary vitamin C (200 mg) and vitamin E (250–500 mg) offers a good management practice to reduce heat stress-related decreases in performance of Japanese quails.


2001 ◽  
Vol 72 (3) ◽  
pp. 529-534 ◽  
Author(s):  
S. Y. Shiau ◽  
L. F. Shiau

AbstractA 10-week feeding trial was conducted to re-evaluate the level of dietary vitamin E (DL- α-tocopheryl acetate) that was adequate for juvenile tilapia Oreochromis niloticus ✕ O. aureus given diets containing two dietary lipid concentrations. Purified diets with eight levels of vitamin E (0, 25, 50, 75, 100, 150, 200, 400 mg/kg diet) at either 50 or 120 g lipid per kg were each given to three replicate groups of tilapia (mean weight: 0·69 (s.e.0·02) g) reared in a closed, recirculating system. Food efficiency and protein deposition were significantly (P < 0·05) higher in fish given 50 mg vitamin E per kg diet and 75 mg/kg diet in the 50 and 120 g lipid per kg groups respectively, compared with fish given the unsupplemented control diet. Mortality of fish was not affected by dietary treatment. Weight gain and liver microsomal ascorbic acid-stimulated lipid peroxidation data analysed by broken-line regression indicated that the optimum dietary vitamin E requirements in juvenile tilapia are 42 to 44 mg vitamin E per kg and 60 to 66 mg vitamin E per kg in 50 and 120 g lipid per kg diets, respectively.


1985 ◽  
Vol 44 (5) ◽  
pp. 1593-1601 ◽  
Author(s):  
Shinichi Yoshida ◽  
Raul Busto ◽  
Brant D. Watson ◽  
Mercedes Santiso ◽  
Myron D. Ginsberg

1995 ◽  
Author(s):  
Joseph Kanner ◽  
Dennis Miller ◽  
Ido Bartov ◽  
John Kinsella ◽  
Stella Harel

Biological oxidations are almost exclusively metal ion-promoted reactions and in ths respect iron, being the most abundant, is the commonly involved. The effect of dietary iron levels on pork, turkey and chick muscle lipid peroxidation and various other related compounds were evaluated. Crossbred feeder pigs were fed to market weight on corn-soy rations containing either 62, 131 or 209 ppm iron. After slaughter, the muscles were dissected, cooked and stored at 4°C. Heavily fortifying swine rations with iron (>200 ppm) increase nn-heme iron (NHI), thiobarbituric acid reactive substances (TBARS), and decrease a-tocopherol in cooked stored pork but did not increase warmed-over aroma (WOA). NHI and TBARS were higher in cooked pork from pigs fed high-iron diets. Liver iron correlated with muscle iron. TBARS were strongly related with WOA. The role of dietary vitamin E and ascorbic acid on Fe-induced in vivo lipid peroxidation in swine was also evaluated. Moderate elevation in iron stores had a marked effect on oxidative stress, especially as indicated by liver TBARS. Supplemental vitamin E, and to a lesser extent vitamin C, protect against this oxidative stress. Unsupplementation of Fe in the regular diet of turkeys did not affect body weight, blood hemoglobin level, or iron pool in the liver or muscle. The reason being that it contained "natural" ~120 mg Fe/kg feed, and this amount is high enough to keep constant the pool of iron in the body, liver or muscle tissues. Only Fe-supplementation with high amounts of Fe (500 ppm) significantly increased turkey blood hemoglobin and total iron in the liver, in 1 out of 3 experiments, but only slightly affects iron pool in the muscles. It seems that the liver accumulates very high concentations of iron and significantly regulates iron concentration in skeletal muscles. For this reason, it was very difficult to decrease muscle stability in turkeys through a diet containing high levels of Fe-supplementation. It was shown that the significant increase in the amount of iron (total and "free") in the muscle by injections with Fe-dextran accelerated its lipid peroxidation rate and decreased its a-tocopherol concentration. The level and metabolism of iron in the muscles affects the intensity of in vivo lipid peroxidation. This process was found to ifluence the turnover and accumulation of a-tocopherol in turkey and chick muscles. Treatments which could significantly decrease the amount and metabolism of iron pool in muscle tissues (or other organs) may affect the rate of lipid peroxidation and the turnover of a-tocopherol. Several defense enzymes were determined and found in the turkey muscle, such as superoxide dismutase, catalase, and glutathione peroxidase. Glutathione peroxidase was more active in muscles with a high trend of lipid peroxidation, lmore so in drumsticks than in breast muscles, or muscles with a low a-tocopherol content. The activity of glutathione peroxidase increased several fold in muscle stored at 4°C. Our work demonstrated that it will be much more practical to increase the stability of muscle tissues in swine, turkeys and chickens during storage and processing by increasing the amount of vitamin E in the diet than by withdrawing iron supplementation.


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