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Lanthanides, also called rare-earth elements, are an interesting group of 15 chemically active, mainly trivalent, f-electronic, silvery-white metals. In fact, lanthanides are not as rare as the name implies, except for promethium, a radioactive artificial element not found in nature. The mean concentrations of lanthanides in the earth's crust are comparable to those of life-important elements like iodine, cobalt and selenium. Many lanthanide compounds show particular magnetic, catalytic and optic properties, and that is why their technical applications are so extensive. Numerous industrial sources enable lanthanides to penetrate into the human body and therefore detailed toxicological studies of these metals are necessary. In the liver, gadolinium selectively inhibits secretion by Kupffer cells and it decreases cytochrome P450 activity in hepatocytes, thereby protecting liver cells against toxic products of xenobiotic biotransformation. Praseodymium ion (Pr3+) produces the same protective effect in liver tissue cultures. Cytophysiological effects of lanthanides appear to result from the similarity of their cationic radii to the size of Ca2+ ions. Trivalent lanthanide ions, especially La3+ and Gd3+, block different calcium channels in human and animal cells. Lanthanides can affect numerous enzymes: Dy3+ and La3+ block Ca2+-ATPase and Mg2+-ATPase, while Eu3+ and Tb3+ inhibit calcineurin. In neurons, lanthanide ions regulate the transport and release of synaptic transmitters and block some membrane receptors, e.g. GABA and glutamate receptors. It is likely that lanthanides significantly and uniquely affect biochemical pathways, thus altering physiological processes in the tissues of humans and animals.
The developing organism lacks many of the cytochrome P450 isoforms detected in the adult, or they are expressed at very low levels. It remains controversial whether P450 gene regulatory mechanisms are present prenatally. As a result, the catalytic function of P450s in fetal tissues has been questioned. The aim of our study was to evaluate CYP: 1A1, 1A2, 2B1/2, 2E1, 3A1 and 3A2 expression in livers of 18- and 20-days-old fetuses, and newborns from untreated and P-naphthoflavone-, phenobarbital-, dexamethasone- or ethanol-treated Sprague-Dawley rats. CYP expressions were evaluated at both tran­scriptional (RT-PCR) and protein (Western blotting) levels. CYP mRNA expressions were detected on day 18 of gestation. CYP: 1A1, 2B1/2 and 3A1 proteins were found on day 18; CYP2E1 protein - on day 20; 1A2 and 3A2 protein - in newborn livers. Studied P450s demonstrated a very low expression in animal tissues before and just after birth but, in most cases, they were inducible. It is concluded that the inductory mechanisms of CYP: 1A1, 2B1/2, 3A1/2 and 2E1 but not CYP1A2, are functional in fetal liver at transcriptional or translational levels. The effects of metabolic activation of CYP1A2 substrates may be reduced in fetuses.
BACKGROUND AND AIMS: Phoenixin (PNX) is one of the last revealed peptide in the rat hypothalamus. PNX so called a satiety molecule, takes part in such processes as the regulation of energy metabolism and also in reproduction. The aim of the study was to examine PNX immunoreactive structures (PNX-ir) and their distribution in the neuroendocrine part of the pig (Sus scrofa domestica) hypothalamus, because PNX was examined only in rodent brains. METHODS: Hypothalamic tissue was prepared by immunohistochemical techniques (immunofluorescence and DAB methods) with using Phoenixin-14 amide (H-079-01; Phoenix). RESULTS: PNX was immunodetected in neurons of the paraventricular (PVN) and supraoptic (SON) nuclei and also in neighbouring areas. PNX-ir cells had oval or multipolar perikarya with 1 to 4 visible primary dendrites. PNX-ir cells in the PVN were situated loosely at dorsal and ventral parts close to the third ventricle, whereas between these parts PNX-ir cells were numbered and clustered. PNX-ir structures with morphology like dendrites and also single fibres covered with varicosities resembled axons were observed in the neuropil of the PVN. PNX-ir cells in the SON were clustered on the medial side of the SON from which narrow band of the PNX-ir perikarya was directed to the lateral side, along the optic tract. PNX-ir perikarya in the SON have similar shapes as in the PVN, but some of them possess short protoplasmic irregular processes, what gives them irregular shapes. In the SON there was not observed immunoreactive structures in neuropil, as above described in the PVN. CONCLUSIONS: This is the first study which demonstrates the presence of PNX in axons. These results suggest that PNX in the PVN and SON may differ in signaling mechanism or acting as molecule-regulated neuroendocrine factor, but multidirectional functions of PNX complicate the understanding of the role played by this neuropeptide and further studies are needed.
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