SHORT-TERM EXPOSURES OF FISH TO PERFLUOROOCTANE SULFONATE: ACUTE EFFECTS ON FATTY ACYL–COA OXIDASE ACTIVITY, OXIDATIVE STRESS, AND CIRCULATING SEX STEROIDS

2005 ◽  
Vol 24 (5) ◽  
pp. 1172 ◽  
Author(s):  
Ken D. Oakes ◽  
Paul K. Sibley ◽  
Jon W. Martin ◽  
Dan D. MacLean ◽  
Keith R. Solomon ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Sex Steroids ◽  
Oxidase Activity ◽  
Perfluorooctane Sulfonate ◽  
Fatty Acyl ◽  
Acute Effects ◽  
Short Term ◽  
Acyl Coa Oxidase

scholarly journals Detection of peroxisomal fatty acyl-coenzyme A oxidase activity

1979 ◽  
Vol 182 (3) ◽  
pp. 779-788 ◽  
Author(s):  
N C Inestrosa ◽  
M Bronfman ◽  
F Leighton
Keyword(s):  
Fatty Acid ◽  
Oxidase Activity ◽  
Subcellular Fractionation ◽  
Fatty Acyl ◽  
O2 Consumption ◽  
H2o2 Generation ◽  
Acyl Coa Oxidase ◽  
Acyl Coenzyme A ◽  
Rate Limiting ◽  
Peroxisomal Fatty Acid

It has been postulated that the peroxisomal fatty acid-oxidizing system [Lazarow & de Duve (1976) Proc. Natl. Acad. Sci. U.S.A. 73, 2043–2046; Lazarow (1978) J. Biol. Chem. 253, 1522–1528] resembles that of mitochondria, except for the first oxidative reaction. In this step, O2 would be directly reduced to H2O2 by an oxidase. Two specific procedures developed to detect the activity of the characteristic enzyme fatty acyl-CoA oxidase are presented, namely polarographic detection of palmitoyl-CoA-dependent cyanide-insensitive O2 consumption and palmitoyl-CoA-dependent H2O2 generation coupled to the peroxidation of methanol in an antimycin A-insensitive reaction. Fatty acyl-CoA oxidase activity is stimulated by FAD, which supports the flavoprotein nature postulated for this enzyme. Its activity increases 7-fold per g wet wt. of liver in rats treated with nafenopin, a hypolipidaemic drug. Subcellular fractionation of livers from normal and nafenopin-treated animals provides evidence for its peroxisomal localization. The stoicheiometry for palmitoyl-CoA-dependent O2 consumption, H2O2 generation and NAD+ reduction is 1 : 1 : 1. This suggests that fatty acyl-CoA oxidase is the rate-limiting enzyme of the peroxisomal fatty acid-oxidizing system.

scholarly journals A sensitive spectrophotometric assay for peroxisomal acyl-CoA oxidase

1985 ◽  
Vol 227 (1) ◽  
pp. 205-210 ◽  
Author(s):  
G M Small ◽  
K Burdett ◽  
M J Connock
Keyword(s):  
Oxidase Activity ◽  
Mouse Liver ◽  
Enzyme Concentration ◽  
Fatty Acyl ◽  
Spectrophotometric Assay ◽  
Acid Oxidase ◽  
Rat Intestine ◽  
Amino Acid Oxidase ◽  
Acyl Coa Oxidase ◽  
First Time

A simple spectrophotometric assay was developed for peroxisomal fatty acyl-CoA oxidase activity. The assay, based on the H2O2-dependent oxidation of leuco-dichlorofluorescein catalysed by exogenous peroxidase, is more sensitive than methods previously described. By using mouse liver samples, cofactor requirements were assessed and a linear relationship was demonstrated between dye oxidation and enzyme concentration. By using this assay on subcellular fractions, palmitoyl-CoA oxidase activity was localized for the first time in microperoxisomes of rat intestine. The assay was also adapted to measure D-amino acid oxidase activity, demonstrating the versatility of this method for measuring activity of other H2O2-producing oxidases.

scholarly journals Identification and purification of a peroxisomal branched chain fatty acyl-CoA oxidase.

1991 ◽  
Vol 266 (36) ◽  
pp. 24676-24683
Author(s):  
P.P. Van Veldhoven ◽  
G. Vanhove ◽  
F. Vanhoutte ◽  
G. Dacremont ◽  
G. Parmentier ◽  
...  
Keyword(s):  
Fatty Acyl ◽  
Acyl Coa Oxidase ◽  
Branched Chain

scholarly journals Neuroprotective Benefits of Exercise and MitoQ on Memory Function, Mitochondrial Dynamics, Oxidative Stress, and Neuroinflammation in D-Galactose-Induced Aging Rats

2021 ◽  
Vol 11 (2) ◽  
pp. 164
Author(s):  
Jae-Hoon Jeong ◽  
Jung-Hoon Koo ◽  
Jang Soo Yook ◽  
Joon-Yong Cho ◽  
Eun-Bum Kang
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Cognitive Impairment ◽  
Nadph Oxidase ◽  
Learning And Memory ◽  
Oxidase Activity ◽  
Mitochondrial Dynamics ◽  
Nadph Oxidase Activity ◽  
Aging Rats ◽  
Positive Effects

Exercise and antioxidants have health benefits that improve cognitive impairment and may act synergistically. In this study, we examined the effects of treadmill exercise (TE) and mitochondria-targeted antioxidant mitoquinone (MitoQ), individually or combined, on learning and memory, mitochondrial dynamics, NADPH oxidase activity, and neuroinflammation and antioxidant activity in the hippocampus of D-galactose-induced aging rats. TE alone and TE combined with MitoQ in aging rats reduced mitochondrial fission factors (Drp1, Fis1) and increased mitochondrial fusion factors (Mfn1, Mfn2, Opa1). These groups also exhibited improved NADPH oxidase activity and antioxidant activity (SOD-2, catalase). TE or MitoQ alone decreased neuroinflammatory response (COX-2, TNF-α), but the suppression was greater with their combination. In addition, aging-increased neuroinflammation in the dentate gyrus was decreased in TE but not MitoQ treatment. Learning and memory tests showed that, contrarily, MitoQ alone demonstrated some similar effects to TE but not a definitive improvement. In conclusion, this study demonstrated that MitoQ exerted some positive effects on aging when used as an isolated treatment, but TE had a more effective role on cognitive impairment, oxidative stress, inflammation, and mitochondria dysfunction. Our findings suggest that the combination of TE and MitoQ exerted no synergistic effects and indicated regular exercise should be the first priority in neuroprotection of age-related cognitive decline.

scholarly journals Oxidative Stress, Glutathione Metabolism, and Liver Regeneration Pathways Are Activated in Hereditary Tyrosinemia Type 1 Mice upon Short-Term Nitisinone Discontinuation

Genes ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 3
Author(s):  
Haaike Colemonts-Vroninks ◽  
Jessie Neuckermans ◽  
Lionel Marcelis ◽  
Paul Claes ◽  
Steven Branson ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Liver Regeneration ◽  
The Body ◽  
Glutathione Metabolism ◽  
Short Term ◽  
Therapeutic Regime ◽  
Tyrosinemia Type 1 ◽  
Hereditary Tyrosinemia

Hereditary tyrosinemia type 1 (HT1) is an inherited condition in which the body is unable to break down the amino acid tyrosine due to mutations in the fumarylacetoacetate hydrolase (FAH) gene, coding for the final enzyme of the tyrosine degradation pathway. As a consequence, HT1 patients accumulate toxic tyrosine derivatives causing severe liver damage. Since its introduction, the drug nitisinone (NTBC) has offered a life-saving treatment that inhibits the upstream enzyme 4-hydroxyphenylpyruvate dioxygenase (HPD), thereby preventing production of downstream toxic metabolites. However, HT1 patients under NTBC therapy remain unable to degrade tyrosine. To control the disease and side-effects of the drug, HT1 patients need to take NTBC as an adjunct to a lifelong tyrosine and phenylalanine restricted diet. As a consequence of this strict therapeutic regime, drug compliance issues can arise with significant influence on patient health. In this study, we investigated the molecular impact of short-term NTBC therapy discontinuation on liver tissue of Fah-deficient mice. We found that after seven days of NTBC withdrawal, molecular pathways related to oxidative stress, glutathione metabolism, and liver regeneration were mostly affected. More specifically, NRF2-mediated oxidative stress response and several toxicological gene classes related to reactive oxygen species metabolism were significantly modulated. We observed that the expression of several key glutathione metabolism related genes including Slc7a11 and Ggt1 was highly increased after short-term NTBC therapy deprivation. This stress response was associated with the transcriptional activation of several markers of liver progenitor cells including Atf3, Cyr61, Ddr1, Epcam, Elovl7, and Glis3, indicating a concreted activation of liver regeneration early after NTBC withdrawal.

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