Hepatotoxicity Caused by Dietary Secondary Products Originating from Lipid Peroxidation

Kanazawa, Kazuki

doi:10.1007/978-1-4899-2626-5_17

Cited by 15 publications

(10 citation statements)

References 52 publications

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“…Fish oil is rich in polyunsaturated fatty acids such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which are necessary to maintain cell membrane fluidity of aquatic animals (Lee & Shiau ). But EPA and DHA are very easy to be oxidized during feed processing and storage, resulting in damage of cellular biomembranes (Kanazawa , ), diet flavour (Simic & Karel ) and animal health deterioration (Hamre et al . ).…”

Section: Introductionmentioning

confidence: 99%

Effect of oxidized fish oil and α-tocopherol on growth, antioxidation status, serum immune enzyme activity and resistance toAeromonas hydrophilachallenge of Chinese mitten crabEriocheir sinensis

Wang

Qin

et al. 2015

Aquacult Nutr

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The impact of dietary a-tocopherol on juvenile Chinese mitten crab Eriocheir sinensis was experimentally evaluated in a 10-week study. Crab were fed with nine diets including three levels of a-tocopherol (0, 100 and 300 mg kg À1 diet) and three levels of fish oil oxidation (fresh, moderate and high) in triplicates. Fresh and moderate oil oxidization enhanced weight gain, but moderate and high oil oxidization lowered survival and feed efficiency. The 100-mg a-tocopherol kg À1 diet resulted in higher hepatopancreas MDA than other a-tocopherol diets. High oil oxidization led to the lowest serum superoxide dismutase (SOD) and glutathione peroxidase (GPH-PX). The serum SOD and GPH-PX activities in crab fed 100 mg a-tocopherol were higher than in those fed other a-tocopherol diets. The diet without a-tocopherol addition lowered lysozyme and phenoloxidase (PO) activities compared to other a-tocopherol diets. Fresh fish oil diet increased PO activity compared to oxidized oils. High oil oxidization caused significantly more mortality than fresh or moderate oxidization after 7-d postchallenge with Aeromonas hydrophila. Supplementation with a-tocopherol significantly enhanced resistance to bacterial infection. This study indicates that a-tocopherol can protect lipid from peroxidation and enhance disease resistance.

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Section: Introductionmentioning

confidence: 99%

Effect of oxidized fish oil and α-tocopherol on growth, antioxidation status, serum immune enzyme activity and resistance toAeromonas hydrophilachallenge of Chinese mitten crabEriocheir sinensis

Wang

Qin

et al. 2015

Aquacult Nutr

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show abstract

Section: Introductionmentioning

confidence: 99%

“…Lipid peroxidation is recognized as being highly deleterious, producing toxic compounds such as fatty acid hydroperoxides, fatty acid hydroxides, aldehydes and hydrocarbons, resulting in damage to cellular biomembranes (Kanazawa 1991(Kanazawa , 1993 and subcellular membranes, such as those of mitochondria, causing several pathological conditions (Watanabe et al 1970;Murai & Andrews 1974;Sakai et al 1989). To counteract this oxidative risk, fish have an endogenous antioxidant defence system (Filho et al 1993), namely radical scavenging enzymes that play an important role in physiological antioxidant protection (Blazer 1982) such as catalase (CAT) and superoxide dismutase (SOD), acting on hydrogen peroxide and superoxide, respectively, and glutathione peroxidase (GPX), which scavenges lipid hydroperoxides (Winston & Di Giulio 1991;Halliwell & Gutteridge 1996).…”

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confidence: 99%

Biomarkers of bone development and oxidative stress in gilthead sea bream larvae fed microdiets with several levels of polar lipids and α-tocopherol

et al. 2014

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Although dietary marine phospholipids are able to improve culture performance of marine fish larvae in a further extend than soybean lecithin, both types of phospholipids (PL) markedly increase oxidative risk. The inclusion of a fat‐soluble antioxidant such as the vitamin E α‐tocopherol could allow a better control of oxidative stress. The objective of this study was to determine the combined effect of graded levels of α‐tocopherol with different levels and sources of krill phospholipids (KPL) and soybean lecithin (SBL) on growth, survival, resistance to stress, oxidative status, bone metabolism‐related genes expression and biochemical composition of sea bream larvae. Sea bream larvae were completely weaned at 16 dph and fed for 30 days seven microdiets with three different levels of PL (0, 40 and 80 g kg−1 diet) and two of α‐tocopherol 1500 and 3000 mg kg−1 diet. Sea bream larvae fed diets without PL supplementation showed the lowest survival, growth and stress resistance, whereas increase in PL, particularly KPL, markedly promoted larval survival and growth. However, feeding SBL markedly increased TBARs and GPX gene expression increasing the peroxidation risk in the larvae. Besides, KPL inclusion improved incorporation of n‐3 HUFA and, particularly, EPA into larval tissues, these fatty acids being positively correlated with the expression of BMP‐4, RUNX 2, ALP, OC and OP genes and to bone mineralization for a given larval size class. The increase in dietary α‐tocopherol tends to improve growth in relation to the n‐3 HUFA levels in the diet, denoting the protective role of this vitamin against oxidation. Indeed, dietary α‐tocopherol decreased the oxidative stress in the larvae as denoted by the reduction in larval TBARs contents and gene expression of SOD and CAT, but not GPX. Thus, increase in dietary α‐tocopherol effectively prevented the formation of free radicals from HUFA, particularly EPA, but did not affect the incidence of bone anomalies or the expression of genes related to osteogenetic processes.

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“…Lipid peroxidation, specifically polyunsaturated fatty acid (PUFA) oxidation is highly deleterious, resulting in damage to cellular biomembranes as a consequence of oxidative deterioration of membrane lipids (Kanazawa, 1991;. In fish, in vivo lipid peroxidation caused by oxygen radicals is a principal cause of several diseases (Kawatsu, 1969;Sakai et al, 1989;Watanabe et al, 1970;Murai and Andrews, 1974).…”

Section: Introductionmentioning

confidence: 99%

Increased activities of hepatic antioxidant defence enzymes in juvenile gilthead sea bream (Sparus aurata L.) fed dietary oxidised oil: attenuation by dietary vitamin E

et al. 2002

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Previously, we had shown that altering the highly unsaturated fatty acid(HUFA)/vitamin E ratios in sea bream (Sparus aurata) livers significantly affected their peroxidation status, with fish fed the diet rich in HUFA and low in vitamin E showing significantly higher values of lipid peroxidation products, without, however, significant effects on liver antioxidant defence enzyme activities. The aim of the present trial was to further characterise the biochemical indicators of peroxidative stress in juvenile sea bream. A high pro-oxidative stress was induced by feeding diets containing around 7% of the dry weight as n-3HUFA. The potential peroxidative stress was increased by oxidising the oil, increasing the peroxide value of the oil some 10-fold. These oils were fed without or with supplemental vitamin E (α-tocopherol acetate at 200 mg.kg -1 dry diet) giving four diets in total. Fish were sampled after 30 and 60 days of feeding the experimental diets. None of the diets had any serious deleterious effects on growth and mortality of the fish during the trial. Similarly, there were few significant effects due to dietary oxidised oil or supplementary vitamin E on liver lipid and fatty acid profiles of livers and, in particular, the proportions of HUFA were not decreased by dietary oxidised oil. The vitamin E content of the liver reflected the vitamin E contents of the diets but was also affected by dietary oxidised oil being reduced by oxidised oil in fish fed diets without supplemental vitamin E but, unexpectedly, increased by oxidised oil in fish fed diets supplemented with vitamin E. Liver TBARS levels were significantly lower in fish fed diets supplemented with vitamin E whereas dietary oxidised oil had no major effects on lipid peroxidation products. Catalase and superoxide dismutase activities were both increased in fish fed dietary oxidised oil and reduced by supplementary vitamin E after 30 days feeding.In contrast glutathione peroxidase was less affected by the diets, and the activities of glutathione-S-transferase and glutathione reductase were only reduced by dietary vitamin E after 60 days of feeding. However, all the enzyme activities were significantly affected by the duration of feeding, but the number of interactions between the three factors (time, oil and vitamin E) showed that the relationships were complicated. In conclusion, the present study showed that feeding diets containing oxidized oil significantly affected the activities of liver antioxidant defence enzymes and that dietary vitamin E partially abrogated these effects.Growth and survival of the fish were relatively unaffected suggesting that the responses in sea bream offered effective protection. However, the duration of feeding the diets of high pro-oxidative stress was observed to have a hitherto unknown effect, possibly the result of an adaptive process, but which requires further investigation.

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Hepatotoxicity Caused by Dietary Secondary Products Originating from Lipid Peroxidation

Cited by 15 publications

References 52 publications

Effect of oxidized fish oil and α-tocopherol on growth, antioxidation status, serum immune enzyme activity and resistance toAeromonas hydrophilachallenge of Chinese mitten crabEriocheir sinensis

Effect of oxidized fish oil and α-tocopherol on growth, antioxidation status, serum immune enzyme activity and resistance toAeromonas hydrophilachallenge of Chinese mitten crabEriocheir sinensis

Biomarkers of bone development and oxidative stress in gilthead sea bream larvae fed microdiets with several levels of polar lipids and α-tocopherol

Increased activities of hepatic antioxidant defence enzymes in juvenile gilthead sea bream (Sparus aurata L.) fed dietary oxidised oil: attenuation by dietary vitamin E

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