Enhancement of flavonoid ability to cross the blood-brain barrier of rats by co-administration with α-tocopherol.

Vitamin E and polyphenols could exhibit a therapeutic role in the treatment of oxidative stress-induced neurodegenerative diseases. Therefore, their ability to cross the blood-brain barrier (BBB) represents an important issue to be explored by different diet combinations. In this study, we have evaluated the ability of α-tocopherol to support epigallocatechin-3-gallate (EGCG), quercetin and rutin to cross the BBB, following oral administration.

Expression and subcellular localization of myogenic regulatory factors during the differentiation of skeletal muscle C2C12 myoblasts.

It is known that the MyoD family members (MyoD, Myf5, myogenin, and MRF4) play a pivotal role in the complex mechanism of skeletal muscle cell differentiation. However, fragmentary information on transcription factor-specific regulation is available and data on their post-transcriptional and post-translational behavior are still missing. In this work, we combined mRNA and protein expression analysis with their subcellular localization.

alpha-Tocopherol affects neuronal plasticity in adult rat dentate gyrus: the possible role of PKCdelta.

Hippocampus dentate gyrus (DG) is characterized by neuronal plasticity processes in adulthood, and polysialylation of NCAM promotes neuronal plasticity. In previous investigations we found that alpha-tocopherol increased the PSA-NCAM-positive granule cell number in adult rat DG, suggesting that alpha-tocopherol may enhance neuronal plasticity. To verify this hypothesis, in the present study, structural remodeling in adult rat DG was investigated under alpha-tocopherol supplementation conditions.

Glucose-6-phosphate dehydrogenase and NADPH-consuming enzymes in the rat olfactory bulb.

The resistance to oxidative stress is a multifactorial reaction involving the clustering of transcriptionally regulated genes. Because glucose-6-phosphate dehydrogenase (G6PD), the principal enzyme responsible for reducing power, is highly expressed in the olfactory bulb (OB), it is of interest to verify whether other enzymes utilizing NADPH are also highly expressed. The level and localization of G6PD- and NADPH-consuming enzymes, such as NADPH-cytochrome P450 oxidoreductase (P450R), glutathione reductase (GR), and NADPH-diaphorase (NADPH-d), were analyzed in the rat olfactory bulb (OB) by quantitative histochemistry and immunohistochemistry.

NADPH-consuming enzymes correlate with glucose-6-phosphate dehydrogenase in Purkinje cells: an immunohistochemical and enzyme histochemical study of the rat cerebellar cortex.

In cerebellum of the adult rat, glucose-6-phosphate dehydrogenase (G6PD) activity is particularly localized in Purkinje cells, showing lower activity in the molecular and granule cell layers. G6PD is the first and rate-limiting step of the hexose monophosphate shunt (HMS), which has the physiological role of providing NADPH for reductive biosynthesis and detoxifying reactions. In this study, we searched for a possible correlation between G6PD and other NADPH-consuming enzymes, such as NADPH-cytochrome P450 reductase (P450R), glutathione reductase (GR) and NADPH-diaphorase (NADPH-d).

Vitamin E affects cell death in adult rat dentate gyrus.

We have previously reported the presence of dying cells in the granule cell layer (GCL) of adult rat dentate gyrus (DG), where neurogenesis occurs. In particular, we found that cell death in the GCL increased in vitamin E deficiency and decreased in vitamin E supplementation. These findings were regarded as related to changes in neurogenesis rate, which in turn was influenced by vitamin E availability; a neuroprotective effect of vitamin E on cell death was also proposed.

Glucose-6-phosphate dehydrogenase expression associated with NADPH-dependent reactions in cerebellar neurons.

This review describes the variation of glucose-6-phosphate dehydrogenase (G6PD) activity in the main neurons of the molecular and granular layers as well as in the deep nuclei of the cerebellum as observed so far by optical and electron microscopy studies. Light microscopy and semiquantitative microphotometry of histochemical staining showed that the highest G6PD activity was expressed by Purkinje cells and neurons of the deep cerebellar nuclei; the elements of the molecular layer showed a diffuse G6PD staining, while the granular layer displayed only scattered G6PD activity. Electron microscopy analysis showed that the basket and stellate cells, as well as the Golgi cells, have a remarkable G6PD activity, while in the granule cells the enzyme was barely detectable.

Alpha-tocopherol, an exogenous factor of adult hippocampal neurogenesis regulation.

In previous work, we found that adult hippocampal neurogenesis in rat is affected by vitamin E deficiency. Because vitamin E deficiency is a complex condition involving numerous biological systems, it is possible that its effect on postnatal new neuron production could be mediated by unknown changes in different factors that in turn play a role in this process. To clarify if vitamin E plays a direct role in regulating hippocampal neurogenesis, we studied the neurogenesis in adult control rats and in adult rats under supplementation with alpha-tocopherol, the most important compound of vitamin E.

Effects of thiocolchicine on axonal cytoskeleton of the rat peroneus nerve.

Thiocolchicine is a colchicine-derivative used in the therapy of some diseases and extensively studied in the field of oncological research as antimitotic agent. Here we studied the activity of thiocolchicine on the cytoskeleton of the peroneus nerve, performing a histological and ultrastructural analysis. We observed a decrease in mean myelinated fiber area in thiocolchicine-treated rats in comparison to controls; this was due to a decrease in mean axoplasm area, while myelin thickness was constant.

Neural precursor proliferation and newborn cell survival in the adult rat dentate gyrus are affected by vitamin E deficiency.

The adult hippocampal neurogenesis is affected by vitamin E deficiency. In the present investigation we examined if neural precursor proliferation, newborn cell survival or both are altered by vitamin E deficiency. 5-Bromo-2'-deoxyuridine (BrdU) was employed as a marker of proliferating cells.

Impairment of neural precursor proliferation increases survival of cell progeny in the adult rat dentate gyrus.

In the present study we show that a reduction in the number of neural precursor cells enhances survival of new granule cells in the dentate gyrus allowing the recovery of the proper granule cell layer structure. To diminish the number of newborn cells methylazoxymethanol (MAM), a toxic agent for proliferating cells, was injected during neonatal life. Proliferation of precursor cells and survival of newborn cells were assessed by BrdU administration to 1-month-old rats when granule cell layer still shows a reduction in granule cell number in treated animals.

Tocopherols enhance neurogenesis in dentate gyrus of adult rats.

In the dentate gyrus of the mammalian hippocampus, neurogenesis carries on throughout postnatal life. The aim of this work was to identify an exogenous control factor of adult neurogenesis. Neurogenesis in the adult dentate gyrus was previously found to be enhanced in vitamin E-deficient rats.

Postnatal development of rat dentate gyrus: effects of methylazoxymethanol administration.

In order to investigate the role of postnatal neurogenesis in granule cell number control in the rat dentate gyrus, we administered Methylazoxymethanol (MAM), a drug able to prevent cells from dividing, on P3, P5, P7, P9, when the most granule cells are produced. The effect of MAM on the number of proliferating precursors and of granule cells was examined at P16 and P90. We used 5-bromo-2'-deoxyuridine administration to label proliferating cells and immunohistochemistry to characterize the cell phenotype using neuron markers TUC 4, PSA-NCAM, Calbindin D28K and glial marker GFAP.