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Potent suppression of the adaptive immune response in mice upon dietary exposure to the potent peroxisome proliferator, perfluorooctanoic acid.
The results clearly demonstrate that oral administration of PFOA prevents both the increases in plaque formations by anti-IgM and -IgG and in serum levels of IgM and IgG normally evoked by such immunization, as well as the possible relevance of this immunosuppression to the alterations in plasma lipids caused by PPs.
Involvement of the peroxisome proliferator-activated receptor alpha in the immunomodulation caused by peroxisome proliferators in mice.
Data indicate that PPARalpha plays a major role in the immunomodulation caused by PPs, with reductions in spleen weight and in the number of splenocytes caused by PP treatment in wild-type mice not observed in PPAR alpha-null mice.
Further evidence for the involvement of inhibition of cell proliferation and development in thymic and splenic atrophy induced by the peroxisome proliferator perfluoroctanoic acid in mice.
Recovery of thymocytes began with increases in the populations in these same phases of the cell cycle, with CD4+CD8+ cells recovering most rapidly, lending further support to the previous hypothesis.
High-dose, short-term exposure of mice to perfluorooctanesulfonate (PFOS) or perfluorooctanoate (PFOA) affects the number of circulating neutrophils differently, but enhances the inflammatory
In addition to suppressing adaptive immunity, high-dose, short-term exposure of mice to either PFOS or PFOA augments inflammatory responses to LPS, a potent activator of innate immunity.
Interactions between brain mitochondria and cytoskeleton: Evidence for specialized outer membrane domains involved in the association of cytoskeleton‐associated proteins to mitochondria in situ and
The surface distribution of several proteins (porin, hexokinase, and two proteins associated with microtubules or actin filaments) on the outer membrane of brain mitochondria was analyzed by
Dietary exposure to perfluorooctanoate or perfluorooctane sulfonate induces hypertrophy in centrilobular hepatocytes and alters the hepatic immune status in mice.
In mice, PFOA- and PFOS-induced hepatomegaly is associated with significant alterations in hepatic histophysiology and immune status, as well as induction of hepatic erythropoiesis.
The atrophy and changes in the cellular compositions of the thymus and spleen observed in mice subjected to short-term exposure to perfluorooctanesulfonate are high-dose phenomena mediated in part by
Comparison of male wild-type 129/Sv mice and the corresponding knock-outs lacking peroxisome proliferator-activated receptor-alpha (PPARalpha) indicated that these effects of PFOS are not strain-dependent, and hepatomegaly is independent of PPARalpha, thymic changes are partially dependent on this receptor, and splenic responses are largely eliminated in its absence.
On the Role of the General Transcription Factor Sp1 in the Activation and Repression of Diverse Mammalian Oxidative Phosphorylation Genes*
Data from transfected Drosophila cells provide the first direct proof for the involvement of Sp1 in the negativeregulation of the ANT2 promoter and as a possible participant in repression of the β-subunit promoter.
The role of thyroid hormone and promoter diversity in the regulation of nuclear encoded mitochondrial proteins.
The findings suggest that nuclear OXPHOS genes are not necessarily expressed in a coordinated manner, and that multiple regulatory circuits might exist which are linked to different physiological stimuli, and the possibility for the existence of disease states linked to regulatory defects.
Expression of glycolytic isoenzymes in activated human peripheral lymphocytes: cell cycle analysis using flow cytometry.
Induction of glycolytic isoenzymes provides an excellent marker of T-cell activation and progression toward DNA synthesis.