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Peroxisome Proliferation (peroxisome + proliferation)
Selected AbstractsPeroxisome Proliferation in Foraminifera Inhabiting the Chemocline: An Adaptation to Reactive Oxygen Species Exposure?,THE JOURNAL OF EUKARYOTIC MICROBIOLOGY, Issue 3 2008JOAN M. BERNHARD ABSTRACT. Certain foraminiferal species are abundant within the chemocline of marine sediments. Ultrastructurally, most of these species possess numerous peroxisomes complexed with the endoplasmic reticulum (ER); mitochondria are often interspersed among these complexes. In the Santa Barbara Basin, pore-water bathing Foraminifera and co-occurring sulfur-oxidizing microbial mats had micromolar levels of hydrogen peroxide (H2O2), a reactive oxygen species that can be detrimental to biological membranes. Experimental results indicate that adenosine triphosphate concentrations are significantly higher in Foraminifera incubated in 16 ,M H2O2 than in specimens incubated in the absence of H2O2. New ultrastructural and experimental observations, together with published results, lead us to propose that foraminiferans can utilize oxygen derived from the breakdown of environmentally and metabolically produced H2O2. Such a capability could explain foraminiferal adaptation to certain chemically inhospitable environments; it would also force us to reassess the role of protists in biogeochemistry, especially with respect to hydrogen and iron. The ecology of these protists also appears to be tightly linked to the sulfur cycle. Finally, given that some Foraminifera bearing peroxisome,ER complexes belong to evolutionarily basal groups, an early acquisition of the capability to use environmental H2O2 could have facilitated diversification of foraminiferans during the Neoproterozoic. [source] Impact of perfluorooctanoic acid on fathead minnow (Pimephales promelas) fatty acyl-coa oxidase activity, circulating steroids, and reproduction in outdoor microcosmsENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 8 2004Ken D. Oakes Abstract This study investigates reproductive impairment and biochemical changes in fathead minnow (Pimephales promelas) exposed for 39 d to varying concentrations of perfluorooctanoic acid (PFOA) under microcosm conditions. While the concentrations tested in this study were much higher than those normally found in the environment, no mortality was associated with PFOA exposure. Only modest changes were observed in condition factor and in relative liver and gonad size. Significant declines in circulating plasma steroids were observed, but these were accompanied by only limited increases in time to first oviposition and decreases in overall egg production. Peroxisome proliferation, as quantified by fatty acyl-CoA oxidase (FAO) activity, was elevated with low PFOA concentrations but attenuated with exposure to higher PFOA doses. Little evidence was seen of differential induction of peroxisome-associated enzyme activity with sex. Oxidative stress, as quantified by the 2-thiobarbituric acid reactive substances (TBARS) assay, was only modestly influenced by PFOA exposure and is not a significant consequence of FAO activity in fathead minnow. Perfluorooctanoic acid appears to be relatively nontoxic at environmentally relevant concentrations but may impact biochemical and reproductive endpoints under conditions associated with environmental spills. [source] Peroxisome proliferator-activated receptor ,,retinoid X receptor agonists induce beta-cell protection against palmitate toxicityFEBS JOURNAL, Issue 23 2007Karine Hellemans Fatty acids can stimulate the secretory activity of insulin-producing beta-cells. At elevated concentrations, they can also be toxic to isolated beta-cells. This toxicity varies inversely with the cellular ability to accumulate neutral lipids in the cytoplasm. To further examine whether cytoprotection can be achieved by decreasing cytoplasmic levels of free acyl moieties, we investigated whether palmitate toxicity is also lowered by stimulating its ,-oxidation. Lower rates of palmitate-induced beta-cell death were measured in the presence of l -carnitine as well as after addition of peroxisome proliferator-activated receptor , (PPAR,) agonists, conditions leading to increased palmitate oxidation. In contrast, inhibition of mitochondrial ,-oxidation by etomoxir increased palmitate toxicity. A combination of PPAR, and retinoid X receptor (RXR) agonists acted synergistically and led to complete protection; this was associated with enhanced expression levels of genes involved in mitochondrial and peroxisomal ,-oxidation, lipid metabolism, and peroxisome proliferation. PPAR,,RXR protection was abolished by the carnitine palmitoyl transferase 1 inhibitor etomoxir. These observations indicate that PPAR, and RXR regulate beta-cell susceptibility to long-chain fatty acid toxicity by increasing the rates of ,-oxidation and by involving peroxisomes in fatty acid metabolism. [source] Differential effects of dihalogenated and trihalogenated acetates in the liver of B6C3F1 miceJOURNAL OF APPLIED TOXICOLOGY, Issue 2 2001J. Kato-Weinstein Abstract Haloacetates are produced in the chlorination of drinking water in the range 10,100 ,g l,1. As bromide concentrations increase, brominated haloacetates such as bromodichloroacetate (BDCA), bromochloroacetate (BCA) and dibromoacetate (DBA) appear at higher concentrations than the chlorinated haloacetates: dichloroacetate (DCA) or trichloroacetate (TCA). Both DCA and TCA differ in their hepatic effects; TCA produces peroxisome proliferation as measured by increases in cyanide-insensitive acyl CoA oxidase activity, whereas DCA increases glycogen concentrations. In order to determine whether the brominated haloacetates DBA, BCA and BDCA resemble DCA or TCA more closely, mice were administered DBA, BCA and BDCA in the drinking water at concentrations of 0.2,3 g l,1. Both BCA and DBA caused liver glycogen accumulation to a similar degree as DCA (12 weeks). The accumulation of glycogen occurred in cells scattered throughout the acinus in a pattern very similar to that observed in control mice. In contrast, TCA and low concentrations of BDCA (0.3 g l,1) reduced liver glycogen content, especially in the central lobular region. The high concentration of BDCA (3 g l,1) produced a pattern of glycogen distribution similar to that in DCA-treated and control mice. This effect with a high concentration of BDCA may be attributable to the metabolism of BDCA to DCA. All dihaloacetates reduced serum insulin levels. Conversely, trihaloacetates had no significant effects on serum insulin levels. Dibromoacetate was the only brominated haloacetate that consistently increased acyl-CoA oxidase activity and rates of cell replication in the liver. These results further distinguish the effects of the dihaloacetates from those of peroxisome proliferators like TCA. Copyright © 2001 John Wiley & Sons, Ltd. [source] The role of hepatic peroxisome proliferator-activated receptors (PPARs) in health and diseaseLIVER INTERNATIONAL, Issue 3 2000Lynn Everett Abstract: The liver has long been known to respond to exposure to certain chemicals with hyperplasia and proliferation of the peroxisomal compartment. This response is now known to be mediated by specific receptors. The peroxisome proliferator-activated receptors (PPARs) were cloned 10 years ago, and in that interval, have been found to serve as receptors for a number of endogenous lipid compounds, in addition to the peroxisome proliferators that originally led to their study. Three receptors, designated the ,, ,, and , receptors, have been found in mammals. PPAR, is the most abundant form found in the liver, with smaller amounts of the , and , forms also expressed there. Kupffer cells, like other macrophages, appear to express the , and , isoforms. Hepatic stellate cells are reported to express the , isoform. PPAR, knock-out mice fail to undergo peroxisome proliferation when challenged with the proliferators. Moreover, they have severe derangements of lipid metabolism, particularly during fasting, indicating that normal function of the alpha receptors is needed for lipid homeostasis. This in turn suggests that inadequate PPAR-mediated responses may contribute to abnormal fatty acid metabolism in alcoholic and non-alcoholic steatohepatitis. Recent information suggests that PPAR, receptors may be important in control of the activation state of the stellate cells, and their repression or inactivation may predispose to hepatic fibrosis. The first approved drug that specifically activates PPAR,, troglitazone, has rarely been found to cause serious liver injury. Although this is likely to represent an idiosyncratic reaction, the medical community will need to be alert to the possibility that activation or blockade of these receptors may cause hepatic dysfunction. [source] | |||||||||||||