Turnover of fatty acyl‐CoA oxidase in the liver of rats fed on a partially hydrogenated marine oil

Horie, Shuchi; Suga, Tetsuya

doi:10.1007/bf02535764

Cited by 19 publications

(7 citation statements)

References 35 publications

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“…zymes [29], the large increase in the number of per. oxisomes in the liver of rats fed with a high-fat diet is mainly due to depressed degradation of peroxisomes in the liver of rats fed with a high-fat diet is mainly due to depressed degradation of pcroxisomes [30].…”

Section: Discussionmentioning

confidence: 98%

“…For instance, the involvement of autophagy in the turnover of peroxisomes in fibroblasts from patients with the Zellweger syndrome recently has been established by us [35] and evidence is accumulating that under certain conditions autophagy of peroxisomes may be selective in that the degradation rate of these organellcs is more rapid than that of other cellular structures [7,9,10,30].…”

Section: Discussionmentioning

confidence: 99%

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Autophagic degradation of peroxisomes in isolated rat hepatocytes

Luiken¹,

Berg²,

Heikoop³

et al. 1992

FEBS Letters

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DegraWion of the peroxisomal enzymes fatty acyl-CoA oxidase and cut&se was studied in hepatocytes isolated from rats treated with clofibrate and from control rats. HepatocyLes were incubated in the absence of amino acids in order to ensure maximal flux through the autophagic pathway and in the presence of cycloheximidc to inhibit protein synthesis, (I) Degradation of the two psroxisomal enzymes in hepatocytes from clofibrate-fed rats, but not in hepatocytes from control rats, was much faster than that of other intracellular enzymes, This increased degradation of the pcroxisomal enzymes was almost completely prevented by 3-methyladeninr, an inhibitor of mscroautophagic squmtration. (2) The increased degradation of the peroxisomal enzymes was also inhibited by a long-chain (Cl6:O) and a very-longchain (C26:O) fatly acid, but not by Cl2:0, a medium-chain fatty acid, or by C&O, a short-chain fatty acid. These results provide direct evidence for the proposal thal autophagic sequestration can be highly selective [( 1987) Exp. Mol. Pathol. 46, 1 l4-1221. It is concluded that preferential aulophagy of peroxisomes is prevented when :hese organclles are supplied with their fatty acid substrates.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Autophagic degradation of peroxisomes in isolated rat hepatocytes

Luiken¹,

Berg²,

Heikoop³

et al. 1992

FEBS Letters

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“…Therefore, some adaptive mechanisms seem to affect differently as the feeding period was extended. Partially hydrogenated marine oils rich in EPA and DHA were reported to increase the activity by reducing the rate of acyl-CoA oxidase degradation (Horie and Suga, 1989). It is worthwhile to consider the effect of fatty acids on acyl-CoA oxidase degradation rate as a possible factor to cause different response of these two oils.…”

Section: Discussionmentioning

confidence: 99%

Stimulation of acyl-CoA oxidase by α-linolenic acid-rich perilla oil lowers plasma triacylglycerol level in rats

Kim

Choi

2005

Life Sciences

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“…This is considered to be due to rapid clearance of PFHeA and PFHA in mice compared with PFCAs with longer carbon chain lengths and long half-life of acyl-CoA oxidase, the enzyme working in rate-limiting step of peroxisomal b-oxidation. 24) Namely, since hepatic concentrations of PFHA and PFHeA were measured 24 h after the final injection, there is a possibility that these two PFCAs once entered the liver, played a role in activation of PPARa, and thereafter cleared from the liver. In the previous study, the potency to induce peroxisomal b-oxidation was in the order of PFNAϾPFOAϾPFHA in the liver of male rats.…”

Section: Accumulation Of Pfcas In the Livermentioning

confidence: 99%

Responses of the Liver to Perfluorinated Fatty Acids with Different Carbon Chain Length in Male and Female Mice:In Relation to Induction of Hepatomegaly, Peroxisomal .BETA.-Oxidation and Microsomal 1-Acylglycerophosphocholine Acyltransferase

Kudo

Suzuki-Nakajima

Mitsumoto

et al. 2006

Biological & Pharmaceutical Bulletin

104

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Perfluorinated fatty acids (PFCAs), straight chain fatty acid analogues of which all aliphatic hydrogens are substituted with fluorine are primarily used as industrial materials, because of their surfactant properties, and their chemical and thermal stability. 1) Of PFCAs, perfluorooctanoic acid (PFOA) was the most widely used as a reactive intermediate in the industrial synthesis of fluoroacrylic esters, and its salts are used as processing aids in the production of fluoropolymer and fluoroelastmers and in other surfactant use. Since PFOA does not undergo biotransformation 2) and accumulates in the environment, [3][4][5] PFOA is found in the serum of not only occupationally exposed workers, 6) but also general populations. 7,8) In this respect, most efforts have been made to study biological and hazardous effects of PFOA in particular, 9) so that toxicological information pertaining to PFCAs is limited largely to PFOA.The previous studies showed that administration of PFOA markedly induced peroxisomal b-oxidation in the liver of male rats, whereas the induction was observed in female rats to an extremely less extent. 10,11) The subsequent study using rats as experimental animals showed that a sex-related difference in the induction by perfluorononanonic acid (PFNA) and perfluoroheptanoic acid (PFHA) was significant whereas the extent was not so striking as that by PFOA and that perfluorodecanoic acid (PFDA) markedly induced peroxisomal b-oxidation without sex-related difference.12) When compared the potency to induce peroxisomal b-oxidation by among PFHA, PFOA, PFNA and PFDA in the liver of male rats, the potency of the induction has been shown to be in the order of PFHAϽPFOAϽPFNAՅPFDA.12) On the basis of the findings from in vitro experiments employing rat hepatocytes, it is likely that the extent of the induction of peroxisomal b-oxidation by PFCAs depends on only concentration of PFCA molecules rather than the difference in their perfluoroalkyl chain length.12,13) Differed from the case of rats, the administration of PFOA to female mice has been shown to markedly induce peroxisomal b-oxidation in the liver to the extent comparable to that of male mice. 11,14) However, no explanation has been made for the mechanism responsible for this observation. Moreover, little information is available about biological effect of PFCAs other than PFOA in the liver of mice. These facts stimulate our interest in studying the response of the liver to PFCAs with different perfluoroalkyl chain lengths.The specific goals of the present study are to ascertain (i) whether there exists perfluoroalkyl chain length-related difference in response of the liver of mice to PFCAs employing inductions of hepatomegaly, peroxisomal b-oxidation and microsomal 1-acylglycerophosphocholine (1-acyl-GPC) acyltransferase as parameters; (ii) the reason why there is no difference in the response of hepatic peroxisomal b-oxidation to PFOA in male and female mice; and (iii) whether there is sex-related difference in the response of hepatic peroxisomal ...

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Turnover of fatty acyl‐CoA oxidase in the liver of rats fed on a partially hydrogenated marine oil

Cited by 19 publications

References 35 publications

Autophagic degradation of peroxisomes in isolated rat hepatocytes

Autophagic degradation of peroxisomes in isolated rat hepatocytes

Stimulation of acyl-CoA oxidase by α-linolenic acid-rich perilla oil lowers plasma triacylglycerol level in rats

Responses of the Liver to Perfluorinated Fatty Acids with Different Carbon Chain Length in Male and Female Mice:In Relation to Induction of Hepatomegaly, Peroxisomal .BETA.-Oxidation and Microsomal 1-Acylglycerophosphocholine Acyltransferase

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