Perinatal development of human blood esterases

Ecobichon, D. J.; Stephens, David S.

doi:10.1002/cpt197314141

Cited by 110 publications

(41 citation statements)

References 10 publications

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“…In humans, serum PON1 activity is minimal before and at birth, but gradually increases after birth, reaching a plateau between 6 and 15 months of age (Augustinsson and Barr, 1963;Ecobichon and Stephens, 1973;Mueller et al, 1983;Cole et al, 2003). In the present study in mice, Pon1 mRNA expression in mouse liver was very low in the fetus, but rapidly increased at birth, reaching adult levels at 15 days of age (Fig.…”

Section: Discussionsupporting

confidence: 50%

Hormonal and Chemical Regulation of Paraoxonases in Mice

Cheng

Klaassen

2012

J Pharmacol Exp Ther

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In humans and rodents, paraoxonase (PON/Pon) 1 expression and activity in livers and serum are higher in females than in males, and some drugs increase paraoxonase's expression. However, the underlining mechanisms of gender-divergent expression and chemical regulation of Pon1 remain largely unknown. The present study determined the regulatory mechanisms contributing to gender-divergent and chemically altered Pon expression in mouse livers. Pon1 mRNA was much more abundant in the livers of mice than other tissues, with higher levels in female livers than male livers at mRNA and protein levels. Pon2 mRNA was ubiquitously expressed in mouse tissues, but minimally in mouse liver. Pon3 mRNA was most abundant in mouse lung and liver and less abundant in other tissues. Pon1 mRNA was lowest in fetal liver, markedly increased at parturition, and remained relatively constant thereafter. Pon2 and Pon3 mRNA are highly expressed in fetal liver and decreased after birth. Male-pattern growth hormone (GH) administration in hypophysectomized and lit/lit mice decreased Pon1 expression. Sex hormones and female-pattern GH administration had no effect on Pon1 expression, indicating the importance of male-pattern GH in regulating Pon1. Aryl hydrocarbon receptor, pregnane X receptor, and NF-E2-related factor activators had no effect on Pon1 mRNA. A constitutive androstane receptor (CAR) activator decreased Pon1 expression in wild-type but not CAR-null mice. In conclusion, Pon1 mRNA was most abundant in adult mouse livers, whereas Pon2 and Pon3 mRNAs were most abundant in fetal mouse livers. Female-predominant Pon1 expression in mouse livers is caused by the inhibitory effects of male-pattern GH secretion, and CAR activation decreases Pon1 expression.

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Section: Discussionsupporting

confidence: 50%

Hormonal and Chemical Regulation of Paraoxonases in Mice

Cheng

Klaassen

2012

J Pharmacol Exp Ther

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“…Studies with chlorpyrifos have indicated that a lower hydrolytic detoxication by PON1 accounts for the differential age-related sensitivity in acute toxicity (Mortensen et al, 1996a;Padilla et al, 2000). The finding of low PON1 activity in neonates (Cole et al, 2003a) suggested that PON1 levels may be even lower before birth, as indeed indicated by data showing a 24% lower activity in premature babies using phenylacetate as a substrate (33-36 weeks of gestation) compared to term babies (Ecobichon and Stephens, 1973). In addition, an expectant mother with low PON1 status would be predicted not to be able to provide protection for her fetus against exposure to some OPs (Cole et al, 2003).…”

Section: Iic5 Paraoxonase (Pon1)mentioning

confidence: 96%

“…Studies in rodents have shown that serum and liver PON1 activity is very low at birth, and increases up to postnatal day 21, with a parallel increase in liver mRNA (Mortensen et al, 1996a;Li et al, 1997;Karanth and Pope, 2000), and similar increases were also seen in transgenic mice expressing either the human PON1 R192 or the PON1 Q192 (Cole et al, 2003c). Studies in humans have also shown that serum PON1 activity is very low at birth and increases over time, reaching a plateau between 6 and 15 months of age (Augustinsson and Barr, 1963;Ecobichon and Stephens, 1973;Mueller et al, 1983;Cole et al, 2003a: Chen et al, 2003. Low PON1 activity during development could represent a relevant risk factor for increased susceptibility to the acute toxicity of certain OP insecticides.…”

Section: Iic5 Paraoxonase (Pon1)mentioning

confidence: 99%

Review of the Toxicology of Chlorpyrifos With an Emphasis on Human Exposure and Neurodevelopment

Eaton¹,

Daroff²,

Autrup³

et al. 2008

Critical Reviews in Toxicology

576

413

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“…However, PON activity at term is approximately half of what it is at age 2 years. 73 Low PON activity relative to HDL cholesterol levels at birth may be part of a nonspecific innate immune system that protects the infant against sepsis as discussed above. However, the persistence of proinflammatory HDL into adulthood may predispose and predict susceptibility to atherosclerosis.…”

Section: Proinflammatory Hdl As a Potential Marker Of Susceptibility mentioning

confidence: 99%

HDL and the Inflammatory Response Induced by LDL-Derived Oxidized Phospholipids

Navab¹,

Berliner²,

Subbanagounder³

et al. 2001

ATVB

410

253

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Abstract-Oxidation of low density lipoprotein (LDL) phospholipids containing arachidonic acid at the sn-2 position occurs when a critical concentration of "seeding molecules" derived from the lipoxygenase pathway is reached in LDL. When this critical concentration is reached, the nonenzymatic oxidation of LDL phospholipids produces a series of biologically active, oxidized phospholipids that mediate the cellular events seen in the developing fatty streak. Normal high density lipoprotein (HDL) contains at least 4 enzymes as well as apolipoproteins that can prevent the formation of the LDL-derived oxidized phospholipids or inactivate them after they are formed. In the sense that normal HDL can prevent the formation of or inactivate these inflammatory LDL-derived oxidized phospholipids, normal HDL is anti-inflammatory. HDL from mice that are genetically predisposed to diet-induced atherosclerosis became proinflammatory when the mice are fed an atherogenic diet, injected with LDL-derived oxidized phospholipids, or infected with influenza A virus. Mice that were genetically engineered to be hyperlipidemic on a chow diet and patients with coronary atherosclerosis, despite normal lipid levels, also had proinflammatory HDL. It is proposed that LDL-derived oxidized phospholipids and HDL may be part of a system of nonspecific innate immunity and that the detection of proinflammatory HDL may be a useful marker of susceptibility to atherosclerosis. (Arterioscler Thromb Vasc Biol. 2001;21:481-488.)Key Words: HDL Ⅲ LDL Ⅲ atherosclerosis Ⅲ oxidized phospholipids T he events involved in fatty streak formation resemble those elicited by mycobacteria. 1 Over the past decade, there has been increasing evidence that this inflammatory response may, in part, be elicited by the oxidation of phospholipids contained in LDL. 2,3 Several oxidized phospholipids that are able to induce the genes and proteins necessary for the cellular response seen in the fatty streak have been identified in mildly oxidized LDL and in lesions of animal models of atherosclerosis. 4 -9 Two of these oxidized phospholipids, 1-palmitoyl-2(5-oxovaleroyl)-sn-glycero-3-phosphorylcholine (POVPC) and 1-palmitoyl-2-glutaroyl-snglycero-3-phosphorylcholine (PGPC), both induced monocytes to bind to endothelial cells. 10 However, PGPC but not POVPC also induced neutrophils to bind to endothelial cells. 10 Indeed, POVPC strongly inhibited lipopolysaccharide-mediated induction of neutrophil binding and expression of E-selectin protein and mRNA. 10 This inhibition by POVPC was mediated by a protein kinase A-dependent pathway that resulted in downregulation of nuclear factor-B-dependent transcription. 10 PGPC, on the other hand, induced both E-selectin and vascular cell adhesion molecule-1 (VCAM-1) expression on endothelial cells. 10 On the basis of studies in Xenopus laevis oocytes, Leitinger et al 10 concluded that POVPC and PGPC bound to different receptors. Furthermore, they demonstrated that at concentrations equal to those present in mildly oxidized LDL, POVPC prevente...

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Perinatal development of human blood esterases

Cited by 110 publications

References 10 publications

Hormonal and Chemical Regulation of Paraoxonases in Mice

Hormonal and Chemical Regulation of Paraoxonases in Mice

Review of the Toxicology of Chlorpyrifos With an Emphasis on Human Exposure and Neurodevelopment

HDL and the Inflammatory Response Induced by LDL-Derived Oxidized Phospholipids

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