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  • Our study has some limitations that should be considered

    2022-09-09

    Our study has some limitations that should be considered when the results are interpreted. First, we did not measure the protein levels of Bax and Bcl2, due to time and budget limitations. Although simultaneous measurements of both mRNA and protein levels are complementary for a better understanding of the gene function, gene expression at mRNA level is still informative and could predict protein expression level (Greenbaum et al., 2003, Guo et al., 2008). Second, no evaluation of neuronal loss and mk-801 lesions was conducted in the present study. Our future research should focus on identifying paraoxon-induced brain damage using histological evaluation to characterize the extent of cellular damage.
    Conclusions Our results showed that the mRNA and protein expression of glial glutamate transporters was increased in the cortex of rats exposed to 0.7mg/kg of paraoxon, while expression of neuronal and glial glutamate transporters in the cortex of animals treated with 1mg/kg of paraoxon was decreased which was coupled with an up-regulation of Bax and down-regulation of Bcl2 mRNA levels. Further investigation is necessary to identify the mechanisms that might contribute to paraoxon-induced down-regulation of glutamate transporters.
    Conflict of interest
    Transparency document
    Acknowledgments This work was financially supported by a research fund (91114) from the Molecular and Cell Biology Research Center of Mazandaran University of Medical Sciences.
    Introduction Vitamin D is a steroid, genomic actions of which are mediated through specific nuclear receptor. Vitamin D synthesis starts by cleavage of the B ring of 7-dehydrocholesterol in the epidermis by ultraviolet radiation. The secosteroid precursor molecule, cholecalciferol or vitamin D3 is created after spontaneous isomerisation. Vitamin D3 is subjected to further hydroxylations to a stable precursor form, i.e. 25 hydroxy-vitamin D3 (25OHD3). Nowadays, it is the global pandemic of vitamin D deficiency and insufficiency that afflicts worldwide more than one billion adults and children and so vitamin D deficiency consequences cannot be underestimated (Holick, 2017). The low levels of vitamin D usually affect bone and skeletal health, mineral homeostasis, however this steroid can act also in diverse tissues (Eyles et al., 2014; Holick, 2007). Growing evidences show association of vitamin D deficiency with a wide range of non-skeletal abnormalities, e.g., cardiovascular disease, cancer, and metabolic disorders (Eyles et al., 2013). Moreover, vitamin D is competent for regulating various pathways essential for brain development, mature brain functioning and homeostasis. 25OHD3 and 1,25(OH)2D3 vitamin D metabolites can cross the blood brain barrier (Gascon-Barre and Huet, 1983; Pardridge et al., 1985). Vitamin D receptors and key enzymes of its metabolism were shown to be expressed in the brain (Eyles et al., 2014). Synthesis of active vitamin D form and its elimination in the brain indicated that vitamin D signaling can involve autocrine and paracrine brain pathways (Eyles et al., 2013). Importantly, difference has been shown in distribution of vitamin D receptors in certain brain regions, i.e. expression of the vitamin D receptors in the hippocampus and prefrontal cortex that are brain regions involved in learning and memory (Cui et al., 2015), and also vitamin D receptors were found in astrocytes (Harms et al., 2011; Langub et al., 2001). 1,25(OH)2D3 downregulated the expression of mRNA for the pore-forming subunits of L-type voltage-gated Ca2+ channels (Brewer et al., 2001). 1,25(OH)2D3 blocked the neuronal uptake of reactive oxygen species, e.g. hydrogen peroxide (Ibi et al., 2001). 1,25(OH)2D pre-treatment can ameliorate the impact of experimental lesions (Chabas et al., 2008; Kajta et al., 2009). So, vitamin D can control Ca2+ transients due to its ability to downregulate L-type voltage-gated Ca2+ channels, contribute to the viability and connectivity of individual neurons and trophic support of developing and mature neurons (Eyles et al., 2013). Vitamin D has neurotrophic and neuroprotective actions, and it can alter neurotransmission and synaptic plasticity (Groves et al., 2014).