The elongation of fatty acids by microsomes and mitochondria from normal and pyridoxine-deficient rat brains

Chauhan, M. S.; Dakshinamurti, K.

doi:10.1007/bf00238910

Cited by 8 publications

(3 citation statements)

References 24 publications

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“…An ad co aalactol ipids were examinaesigniiccu deposition of brain g ti on of stear 1 c acid and corn noPernan an ds n erv on i thecil long found were crease in the contents 119 In ridoxine deficient chain (15,16). This was s rel atstemo is py d in fatty acid elongation sy ode ro i d i sm rat brain, which was similar to that ridoxine-de pficient rats y (17,18). Thus, the CNS myei i n of pyridoxine-deficient is qualitatively and quantitatively different from that i not pyridoxine-supplemented controls.…”

Section: / Dakshinamurti Paulose and Sioŵsupporting

confidence: 68%

Neurobiology of Pyridoxine

Dakshinamurti

1982

Advances in Nutritional Research

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Pyridoxal 5'-phosphate (PLP) is the major coenzymatic form of pyridoxine. There are over one hundred known pyridoxal 5'-phosphate-dependent reactions, most of which are involved in the metabolism of various amino acids . Pyridoxamine 5'-phosphate can function in aminotransf erase reactions by the cyclic regeneration of the two active phosphate forms. Pyridoxal 5'-phosphate-dependent reactions studied in the nervous system are involved in the catabolism of various amino acids.The putative neurotransmitters , dopamine, norepinephrine , serotonin , histamine , aminobutyric acid and taurine , as well as the sphingoiipids and poly amines are synthesized by PLP-dependent enzymes. Of these enzymes, three ( glutamic acid decarboxylase , 5-hydroxytryptophan decarboxylase and crnithine decarboxylase) seem to have crucial roles (Fig. '). The clinical effects of pyridoxine deficiency can be explained on the basis of the known decreases in the activities of these enzymes (1). EXPERIMENTAL PYRIDOXINE DEFICIENCY IN THE NEONATE RATDakshinamurti and Stephens ( 2) first reported the production of congenital pyridoxine deficiency .Our observations extended the "chronic fetal distress" hypothesis of Gruenwald ( 3) to include effects on the development of the central nervous system. We later showed that a deficiency of pyridoxine in rat pups could be produced by depriving the dam of dietary pyridoxine during lactation (4). Such a deficiency has been characterized using biochemical and electrophysiological parameters. The electroencephalogram (EEG)

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Section: / Dakshinamurti Paulose and Sioŵsupporting

confidence: 68%

Neurobiology of Pyridoxine

Dakshinamurti

1982

Advances in Nutritional Research

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“…Similarly, Tsuge et al clearly showed that the activity of Δ-6 desaturase was significantly lower (∼64%) in rats fed a pyridoxine-deficient diet compared to the pair-fed control group. A direct effect of pyridoxine status on fatty acid elongation in microsomes and mitochondria in rat brains has been shown . Accordingly, impaired fatty acid desaturation and elongation was apparent in rats receiving pyridoxine-deficient diets …”

Section: Discussionmentioning

confidence: 98%

“…A direct effect of pyridoxine status on fatty acid elongation in microsomes and mitochondria in rat brains has been shown. 35 Accordingly, impaired fatty acid desaturation and elongation was apparent in rats receiving pyridoxine-deficient diets. 9 However, in Atlantic salmon, 16 it was reported that the desaturation and elongation of [1-14 C]18:3n-3 in liver following intraperitoneal injection was not affected by dietary pyridoxine level.…”

Section: ■ Discussionmentioning

confidence: 99%

Effects of Dietary Vitamin B₆ Supplementation on Fillet Fatty Acid Composition and Fatty Acid Metabolism of Rainbow Trout Fed Vegetable Oil Based Diets

Senadheera

Turchini

Thanuthong

et al. 2012

J. Agric. Food Chem.

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Fish oil replacement in aquaculture feeds results in major modifications to the fatty acid makeup of cultured fish. Therefore, in vivo fatty acid biosynthesis has been a topic of considerable research interest. Evidence suggests that pyridoxine (vitamin B(6)) plays a role in fatty acid metabolism, and in particular, the biosynthesis of LC-PUFA has been demonstrated in mammals. However, there is little information on the effects of dietary pyridoxine availability in fish fed diets lacking LC-PUFA. This study demonstrates a relationship between dietary pyridoxine supplementation and fatty acid metabolism in rainbow trout. In particular, the dietary pyridoxine level was shown to modulate and positively stimulate the activity of the fatty acid elongase and Δ-6 and Δ-5 desaturase enzymes, deduced by the whole-body fatty acid balance method. This activity was insufficient to compensate for a diet lacking in LC-PUFA but does highlight potential strategies to maximize this activity in cultured fish, especially when fish oil is replaced with vegetable oils.

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Synthesis of α‐hydroxy stearyl coenzyme A

Chauhan

Dakshinamurti

1980

Lipids

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The elongation of fatty acids by microsomes and mitochondria from normal and pyridoxine-deficient rat brains

Cited by 8 publications

References 24 publications

Neurobiology of Pyridoxine

Neurobiology of Pyridoxine

Effects of Dietary Vitamin B₆ Supplementation on Fillet Fatty Acid Composition and Fatty Acid Metabolism of Rainbow Trout Fed Vegetable Oil Based Diets

Synthesis of α‐hydroxy stearyl coenzyme A

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The elongation of fatty acids by microsomes and mitochondria from normal and pyridoxine-deficient rat brains

Cited by 8 publications

References 24 publications

Neurobiology of Pyridoxine

Neurobiology of Pyridoxine

Effects of Dietary Vitamin B6 Supplementation on Fillet Fatty Acid Composition and Fatty Acid Metabolism of Rainbow Trout Fed Vegetable Oil Based Diets

Synthesis of α‐hydroxy stearyl coenzyme A

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Effects of Dietary Vitamin B₆ Supplementation on Fillet Fatty Acid Composition and Fatty Acid Metabolism of Rainbow Trout Fed Vegetable Oil Based Diets