Exposure to DEHP decreased four fatty acid levels in plasma of prepartum mice

Ryosuke Nakashima, Yumi Hayashi, Khalequzzaman Md., Xiaofang Jia, Dong Wang, Hisao Naito, Yuki Ito, Michihiro Kamijima, Frank J. Gonzalez, Tamie Nakajima

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Maternal exposure to di(2-ethylhexyl) phthalate (DEHP) decreased the plasma triglyceride in prepartum mice. To identify the fatty acid (FA) species involved and to understand the underlying mechanisms, pregnant Sv/129 wild-type (m. PPARα), peroxisome proliferator-activated receptor α-null (. Pparα-null) and humanized PPARα (h. PPARα) mice were treated with diets containing 0%, 0.01%, 0.05% or 0.1% DEHP. Dams were dissected on gestational day 18 together with fetuses, and on postnatal day 2 together with newborns. n-3/n-6 polyunsaturated, saturated, and monounsaturated FAs in maternal plasma and in liver of wild-type offspring, and representative enzymes for FA desaturation and elongation in maternal liver, were measured. The plasma levels of linoleic acid, α-linolenic acid, palmitic acid and oleic acid were higher in the pregnant control m. PPARa mice than in Ppara-null and h. PPARa mice. DEHP exposure significantly decreased the levels of these four FAs only in pregnant m. PPARα mice. Plasma levels of many FAs were higher in pregnant mice than in postpartum ones in a genotype-independent manner, while it was lower in the livers of fetuses than pups. DEHP exposure slightly increased hepatic arachidonic acid, α-linolenic acid, palmitoleic acid and oleic acid in fetuses, but not in pups. However, DEHP exposure did not clearly influence FA desaturase 1 and 2 nor elongase 2 and 5 expressions in the liver of all maternal mice. Taken together, the levels of plasma four FAs with shorter carbon chains were higher in pregnant m. PPARα mice than in other genotypes, and DEHP exposure decreased these specific FA concentrations only in m. PPARα mice, similarly to triglyceride levels.

Original languageEnglish
Pages (from-to)52-60
Number of pages9
JournalToxicology
Volume309
DOIs
Publication statusPublished - 05-07-2013

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Peroxisome Proliferator-Activated Receptors
Fatty Acids
Plasmas
Liver
Oleic Acid
Triglycerides
Fetus
Fatty Acid Desaturases
Mothers
alpha-Linolenic Acid
Palmitic Acid
Nutrition
Genotype
Arachidonic Acid
Dams
phthalic acid
Maternal Exposure
Carbon
Postpartum Period
Diet

All Science Journal Classification (ASJC) codes

  • Toxicology

Cite this

Nakashima, R., Hayashi, Y., Md., K., Jia, X., Wang, D., Naito, H., ... Nakajima, T. (2013). Exposure to DEHP decreased four fatty acid levels in plasma of prepartum mice. Toxicology, 309, 52-60. https://doi.org/10.1016/j.tox.2013.04.010
Nakashima, Ryosuke ; Hayashi, Yumi ; Md., Khalequzzaman ; Jia, Xiaofang ; Wang, Dong ; Naito, Hisao ; Ito, Yuki ; Kamijima, Michihiro ; Gonzalez, Frank J. ; Nakajima, Tamie. / Exposure to DEHP decreased four fatty acid levels in plasma of prepartum mice. In: Toxicology. 2013 ; Vol. 309. pp. 52-60.
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Nakashima, R, Hayashi, Y, Md., K, Jia, X, Wang, D, Naito, H, Ito, Y, Kamijima, M, Gonzalez, FJ & Nakajima, T 2013, 'Exposure to DEHP decreased four fatty acid levels in plasma of prepartum mice', Toxicology, vol. 309, pp. 52-60. https://doi.org/10.1016/j.tox.2013.04.010

Exposure to DEHP decreased four fatty acid levels in plasma of prepartum mice. / Nakashima, Ryosuke; Hayashi, Yumi; Md., Khalequzzaman; Jia, Xiaofang; Wang, Dong; Naito, Hisao; Ito, Yuki; Kamijima, Michihiro; Gonzalez, Frank J.; Nakajima, Tamie.

In: Toxicology, Vol. 309, 05.07.2013, p. 52-60.

Research output: Contribution to journalArticle

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T1 - Exposure to DEHP decreased four fatty acid levels in plasma of prepartum mice

AU - Nakashima, Ryosuke

AU - Hayashi, Yumi

AU - Md., Khalequzzaman

AU - Jia, Xiaofang

AU - Wang, Dong

AU - Naito, Hisao

AU - Ito, Yuki

AU - Kamijima, Michihiro

AU - Gonzalez, Frank J.

AU - Nakajima, Tamie

PY - 2013/7/5

Y1 - 2013/7/5

N2 - Maternal exposure to di(2-ethylhexyl) phthalate (DEHP) decreased the plasma triglyceride in prepartum mice. To identify the fatty acid (FA) species involved and to understand the underlying mechanisms, pregnant Sv/129 wild-type (m. PPARα), peroxisome proliferator-activated receptor α-null (. Pparα-null) and humanized PPARα (h. PPARα) mice were treated with diets containing 0%, 0.01%, 0.05% or 0.1% DEHP. Dams were dissected on gestational day 18 together with fetuses, and on postnatal day 2 together with newborns. n-3/n-6 polyunsaturated, saturated, and monounsaturated FAs in maternal plasma and in liver of wild-type offspring, and representative enzymes for FA desaturation and elongation in maternal liver, were measured. The plasma levels of linoleic acid, α-linolenic acid, palmitic acid and oleic acid were higher in the pregnant control m. PPARa mice than in Ppara-null and h. PPARa mice. DEHP exposure significantly decreased the levels of these four FAs only in pregnant m. PPARα mice. Plasma levels of many FAs were higher in pregnant mice than in postpartum ones in a genotype-independent manner, while it was lower in the livers of fetuses than pups. DEHP exposure slightly increased hepatic arachidonic acid, α-linolenic acid, palmitoleic acid and oleic acid in fetuses, but not in pups. However, DEHP exposure did not clearly influence FA desaturase 1 and 2 nor elongase 2 and 5 expressions in the liver of all maternal mice. Taken together, the levels of plasma four FAs with shorter carbon chains were higher in pregnant m. PPARα mice than in other genotypes, and DEHP exposure decreased these specific FA concentrations only in m. PPARα mice, similarly to triglyceride levels.

AB - Maternal exposure to di(2-ethylhexyl) phthalate (DEHP) decreased the plasma triglyceride in prepartum mice. To identify the fatty acid (FA) species involved and to understand the underlying mechanisms, pregnant Sv/129 wild-type (m. PPARα), peroxisome proliferator-activated receptor α-null (. Pparα-null) and humanized PPARα (h. PPARα) mice were treated with diets containing 0%, 0.01%, 0.05% or 0.1% DEHP. Dams were dissected on gestational day 18 together with fetuses, and on postnatal day 2 together with newborns. n-3/n-6 polyunsaturated, saturated, and monounsaturated FAs in maternal plasma and in liver of wild-type offspring, and representative enzymes for FA desaturation and elongation in maternal liver, were measured. The plasma levels of linoleic acid, α-linolenic acid, palmitic acid and oleic acid were higher in the pregnant control m. PPARa mice than in Ppara-null and h. PPARa mice. DEHP exposure significantly decreased the levels of these four FAs only in pregnant m. PPARα mice. Plasma levels of many FAs were higher in pregnant mice than in postpartum ones in a genotype-independent manner, while it was lower in the livers of fetuses than pups. DEHP exposure slightly increased hepatic arachidonic acid, α-linolenic acid, palmitoleic acid and oleic acid in fetuses, but not in pups. However, DEHP exposure did not clearly influence FA desaturase 1 and 2 nor elongase 2 and 5 expressions in the liver of all maternal mice. Taken together, the levels of plasma four FAs with shorter carbon chains were higher in pregnant m. PPARα mice than in other genotypes, and DEHP exposure decreased these specific FA concentrations only in m. PPARα mice, similarly to triglyceride levels.

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