Joint effects of gamma radiation and zinc on duckweed Lemna minor L.

When assessing the consequences of combined chemical and radiation pollution on bodies of water, it is important to take into account the interaction of different factors, especially the possible synergistic increase in the toxic effect on growth, biochemical and physiological processes of living organisms. In this work, we studied the combined effect of γ-radiation and zinc on freshwater duckweed Lemna minor L. Irradiated plants (doses were 18, 42, and 63 Gy) were placed on a medium with an excess of zinc (3.15, 6.3, 12.6 µmol/L) for 7 days. Our results showed that the accumulation of zinc in tissues increased in irradiated plants when compared to non-irradiated plants. The interaction of factors in assessing their effect on the growth rate of plants was most often additive, but there was also a synergistic increase in the toxic effect at a zinc concentration of 12.6 µmol/L and irradiation at doses of 42 and 63 Gy. When comparing the combined and separate effects of gamma radiation and zinc, it was found that a reduction in the area of fronds (leaf-like plates) was caused exclusively due to the effects of radiation. Zinc and γ-radiation contributed to the enhancement of membrane lipid peroxidation. Irradiation stimulated the production of chlorophylls a and b, as well as carotenoids.

Hopping magnetotransport of the band-gap tuning Cu2Zn(Sn x Ge1-x )Se4 crystals.

Resistivity, ρ(T, x), of Cu2Zn(Sn x Ge1-x )Se4 (CZTGeSe) single crystals with x = 0-1, investigated at temperatures between T ~ 10-320 K, exhibits an activated character within the whole temperature range, attaining a minimum at x = 0.47. Magnetoresistance (MR) of CZTGeSe with x = 0.26, 0.47 and 0.64 is positive (pMR) in all measured fields of B up to 20 T at any T between ~40-320 K, whereas MR of samples with x = 0 and 1 contains a negative contribution (nMR). The dependence of ρ(T) at B = 0 gives evidence for a nearest-neighbor hopping (NNH) conductivity in high-temperature intervals within T ~ 200-320 K depending on x, followed by the Mott variable-range hopping (VRH) charge transfer with lowering temperature. The pMR law of lnρ(B) [Formula: see text] B (2) is observed in both hopping conductivity regimes above, provided that the nMR contribution is absent or saturated. Analysis of the ρ(T) and MR data has yielded the values of the NNH activation energy and the VRH characteristic temperature, as well as those of the acceptor band width, the acceptor concentration, the localization radii of holes and the density of the localized states (DOS) at the Fermi level. All the parameters above exhibit a systematic non-monotonous dependence on x. Their extremums, lying close to x = 0.64, correspond to the minimum of a lattice disorder along with the maximum of DOS and of the acceptor concentration, as well as a highest proximity to the metal-insulator transition.

Fermi resonance in the phonon spectra of quaternary chalcogenides of the type Cu2ZnGeS4.

The experimental resonant and non-resonant Raman scattering spectra of the kesterite structural modification of Cu2ZnGeS4 single crystals are reported. The results are compared with those calculated theoretically within the density functional perturbation theory. For the majority of lines a good agreement (within 2-5 cm(-1)) is established between experimental and calculated mode frequencies. However, several dominant spectral lines, in particular the two intense fully symmetric modes, are found to deviate from the calculated values by as much as 20 cm(-1). A possible reason for this discrepancy is found to be associated with the Fermi resonant interaction between one and two-phonon vibrational excitations. The modelling of spectra, which takes into account the symmetry of interacting states, allows a qualitative description of the observed experimental findings. Due to the similarity of the vibrational spectra of Cu2A (II) B (IV) S4 (A = Zn, Mn, Cd; B = Sn, Ge, Si) chalcogenides, Fermi resonance is argued to be a general phenomenon for this class of compounds.

Can encapsulation lengthen the shelf-life of probiotic bacteria in dry products?

This study evaluated the use of microencapsulation to maintain probiotic Lactobacillus rhamnosus GG (LGG) viability during exposure to detrimentally high levels of water activity. Freeze-dried LGG was mixed into a whey protein solution and sprayed onto a core particle. A second batch was prepared by applying an extra layer of palm oil onto the LGG encapsulates. Viability of the LGG preparations was measured over time in an accelerated shelf-life study at 37 degrees C which included exposure to different water activities (a(w)=0.15 or 0.7), ambient oxygen, and incorporation of the probiotic in infant formula powder. Results showed that a high water activity (0.7) was detrimental to the survival of unencapsulated LGG, yielding more than a 10 log(10) loss in cell viability within 2 weeks. The presence of oxygen and infant formula conferred no additional effects. Encapsulation of LGG did not improve the survival of this strain under the conditions tested here. Although encapsulation is often mentioned as a quick-fix for preserving probiotic viability in dry and semi-dry products, more studies are needed which validate the broader potential of this approach at different shelf-life expectancies, water activities, and product matrices.

The role of catecholamines in the prolactin release induced by salsolinol.

Salsolinol (1,2,3,4-tetrahydro-6,7-dihydroxy-1-methylisoquinoline) is an endogenous prolactin releasing agent. Its action can be inhibited by another isoquinoline, 1-methyl-3,4-dihydroisoquinoline (1MeDIQ), which has a strong norepinephrine releasing activity. Salsolinol does not alter the dopamine release in median eminence in vitro, providing evidence for the lack of interaction with presynaptic D2 dopamine receptors. At the same time, lack of norepinephrine transporter abolishes salsolinol's action. Salsolinol decreases tissue level of dopamine and increases norepinephrine to dopamine ratio in organs innervated by the sympathetic nervous system indicating a possible decrease of norepinephrine release. Enzymes of catecholamine synthesis and metabolism are probably also not the site of action of salsolinol. In summary, based upon all of these observations a physiologically relevant interplay might exist between the sympatho-neuronal system and the regulation of prolactin release.

The peripheral noradrenergic terminal as possible site of action of salsolinol as prolactoliberin.

Salsolinol, an endogenous isoquinoline, induces selective prolactin release in rats [Tóth, B.E., Homicskó, K., Radnai, B., Maruyama, W., DeMaria, J.E., Vecsernyés, M., Fekete, M.I.K., Fülöp, F., Naoi, M., Freeman, M.E., Nagy, G.M., 2001. Salsolinol is a putative neurointermediate lobe prolactin releasing factor. J. Neuroendocrinol. 13, 1042-1050]. The possible role of dopaminergic and adrenergic signal transduction was investigated to learn the mechanism of this action. The effect of salsolinol (10mg/kg i.v.) was inhibited by reserpine treatment (2.5mg/kg i.p.) and reinstated by pretreatment with monoamine oxidase inhibitor (pargyline 75 mg/kg i.p.). Salsolinol did not affect the in vitro release of dopamine (DA) in the median eminence, and did not inhibit the L-DOPA induced increase of DA level in the median eminence. 1-Methyl dihydroisoquinoline (1MeDIQ) is an antagonist of salsolinol induced prolactin release and causes increase in plasma NE level [Mravec, B., Bodnár, I., Fekete, M.I.K., Nagy, G.M., Kvetnansky, R., 2004. An antagonist of prolactoliberine induces an increase in plasma catecholamine levels in the rat. Autonom. Neurosci. 115, 35-40]. Using tissue catecholamine contents as indicators of the interaction between salsolinol and 1MeDIQ we found no interaction between these two agents to explain the changes in prolactin release in the median eminence, lobes of the pituitary, superior cervical and stellate ganglion. Increasing doses of salsolinol caused a dose dependent decrease of tissue dopamine concentration and increase of NE/DA ratio in the salivary gland, atrium and spleen. These changes of DA level and NE/DA ratio run parallel in time with the increase of prolactin release. 1MeDIQ antagonized the increase of prolactin release and decrease of tissue DA content caused by salsolinol. Neither this increase of prolactin secretion nor the decrease of DA level in spleen could be demonstrated in NE transporter (NET) knock out mice. The results presented argue for the possible role of peripheral norepinephrine release as a target for salsolinol in its action releasing prolactin. The dominant role of norepinephrine transporter may be suggested.

Formalin attenuates the stress-induced increase in plasma epinephrine levels.

Subcutaneous (s.c.) injection of formalin into rats is frequently used as a painful stressor that produces a three-phase nociceptive response. We have shown previously that s.c. administered formalin (0.2 ml of 4% solution per 100 g body weight) unexpectedly attenuated the increase of plasma epinephrine levels in rats exposed to exteroceptive stressors (handling, immobilisation). To clarify the mechanism(s) responsible for this phenomenon, the effect of formalin applications on epinephrine plasma levels was investigated in various experimental conditions. Subcutaneous application of formalin combined with exposures of animals to an interoceptive stressor, insulin-induced hypoglycaemia, significantly attenuated the stress-induced increase in plasma epinephrine levels, whereas plasma norepinephrine levels remained highly elevated. Moreover, administration of formalin to unstressed animals also manifested signs of an attenuated epinephrine secretion. Interestingly, intraperitoneal administration of formalin did not reduce the elevated levels of plasma epinephrine. We suggest that formalin attenuates epinephrine secretion from the adrenal medulla most probably via irritation of s.c. somatosensory receptors. We hypothesise that the irritation of the primary sensory afferents fibres might reduce the activity of the sympathetic preganglionic neurones innervating adrenal medullary chromaffin cells. Further investigations are required to establish whether the observed reduction of epinephrine secretion from the adrenal medulla is controlled by either spinal or supraspinal neuronal circuits.

Inhibitory effect of formalin administration on immobilization-induced epinephrine release.

Injection of formalin is used as a classical painful stressor that produces a biphasic nociceptive response consisting of a 1- to 10-min early phase and a later phase 30 to 240 min after injection. The period between these two phases, called "interphase," is characterized by attenuated nociception. We evaluated the response of catecholamine plasma levels to formalin-induced pain stress with special attention to these three time periods. Subcutaneous injection of 4% formalin (0.2 mL/100 g bw) into the hind limb produced a slight reduction of plasma epinephrine levels in the first 15 min, which was followed by a significant increase that remained high up to 120 min after injection. Norepinephrine levels increased immediately after injections and remained high from 30 until 120 min. To test the effect of formalin injection in a stressful condition, we exposed animals to 2 h immobilization stress. In the first experiment, formalin was injected before the start of immobilization. A significant decrease of plasma epinephrine levels was measured up to 25 min post-injection, whereas plasma norepinephrine levels remained high. A second formalin injection during immobilization was as effective as the first one: It depleted plasma epinephrine levels from 5 to 15 min post-injection without significant changes in norepinephrine levels. In the second experiment, formalin given after the beginning of immobilization produced a significant decrease of epinephrine levels 15 min after the injection and produced a significant increase 60 min after injection. The plasma norepinephrine levels were significantly increased by 40 min post-injection. The data show that the inhibitory process during the interphase of formalin test is able to significantly decrease epinephrine release not only during basal conditions but also during exposure to a severe stressor, such as immobilization without suppression of plasma norepinephrine levels.

Pivotal role of an endogenous tetrahydroisoquinoline, salsolinol, in stress- and suckling-induced release of prolactin.

In mammals, the role of a prolactin-releasing factor (PRF) in the acute changes of prolactin (PRL) secretion that usually occur after challenges (e.g., suckling stimulus or stress) of homeostasis has been suspected for a long time. We have recently observed that 1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, salsolinol (SAL), produced by the hypothalamus and the neuro-intermediate lobe (NIL) of the pituitary gland, can selectively release PRL from the anterior lobe (AL). Moreover, binding sites for SAL have been detected in areas like median eminence, NIL, and AL. It has been proposed that SAL is a putative endogenous PRF. We have also found that a structural analogue of SAL, 1-methyl-3,4-dihydroisoquinoline (1MeDIQ), is able to block dose-dependently SAL-, suckling-, and immobilization (IMO) stress-induced release of PRL without having any influence on alpha-methyl-p-tyrosine (alphaMpT)-induced PRL responses. Neither SAL nor 1MeDIQ has any effect on alpha-melanocyte-stimulating hormone (alphaMSH), adrenocorticotrophic hormone (ACTH), beta-endorphin (beta-END) and arginine-vasopressin (AVP) secretion. Moreover, SAL-induced PRL response was attenuated in male rats pretreated with dexamethasone (DEX). These results strongly suggest that SAL has an important role in the regulation of PRL release induced by physiologic and environmental stimuli; therefore, it can be considered as the strongest candidate for being the PRF in the hypothalamo-hypophysial system. Our findings also indicate that the adrenal steroids may play an inhibitory feedback role in SAL-mediated PRL response.

Stress- as well as suckling-induced prolactin release is blocked by a structural analogue of the putative hypophysiotrophic prolactin-releasing factor, salsolinol.

Prolactin is secreted from the anterior lobe of the pituitary gland in response both to suckling and to stress. We recently observed that 1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (salsolinol), produced in the neurointermediate lobe of the pituitary gland, as well as in the medial basal hypothalamus, can selectively release prolactin from the anterior pituitary. Therefore, it has been proposed that salsolinol is a putative endogenous prolactin-releasing factor (PRF). Here, we report that one structural analogue of salsolinol, 1-methyl-3,4-dihydroisoquinoline (1MeDIQ), can block salsolinol-induced release of prolactin, but does not affect prolactin release in response to thyrotropin releasing hormone (TRH), alpha-methyl-p-tyrosine (alpha MpT) (an inhibitor of tyrosine hydroxylase), domperidone (a D(2) dopamine receptor antagonist), or 5-hydroxytryptophan (5-HTP), a precursor of serotonin). 1MeDIQ profoundly inhibited suckling-, immobilization-, as well as formalin-stress induced prolactin release without any influence on corticosterone secretion. The 1MeDIQ-induced reduction in prolactin response to immobilization stress was dose-dependent. These results suggest that salsolinol can play a pivotal role in the regulation of prolactin release induced by either physiological (suckling) or environmental (stress) stimuli.

Neurons containing tuberoinfundibular peptide of 39 residues project to limbic, endocrine, auditory and spinal areas in rat.

Accumulating evidence suggests that tuberoinfundibular peptide of 39 residues (TIP39) may be the endogenous ligand of the parathyroid hormone 2 receptor. The vast majority of TIP39-containing neurons are localized in two regions, the subparafascicular area at the thalamic-midbrain junction, and the medial paralemniscal nucleus in the rostral pons. In contrast to the restricted localization of TIP39-containing cell bodies, TIP39-containing fibers have a widespread distribution. TIP39 neurons were lesioned electrolytically to determine the origin of TIP39-containing fibers within different parts of the rat CNS. Following bilateral lesions of the medial subparafascicular area including the subparafascicular nucleus, TIP39-immunoreactive fibers almost completely disappeared from forebrain regions including the anterior limbic cortical areas, the shell and cone portions of the nucleus accumbens, the lateral septum, the bed nucleus of the stria terminalis, the amygdaloid nuclei, the fundus striati, the subiculum, the thalamic paraventricular nucleus, and the hypothalamic paraventricular, dorsomedial and arcuate nuclei. Unilateral lesions of the medial and the lateral subparafascicular area demonstrated that the projections are ipsilateral and that medial lesions produce higher reductions in the density of TIP39 fibers except in the amygdala and the hypothalamus. Following lesions of the medial paralemniscal nucleus, TIP39-immunoreactive fibers disappeared from the medial geniculate body, the periaqueductal gray, the deep layers of the superior colliculus, the external cortex of the inferior colliculus, the cuneiform nucleus, the nuclei of the lateral lemniscus, the lateral parabrachial nucleus, the locus coeruleus, the subcoeruleus area, the medial nucleus of the trapezoid body, the periolivary nuclei, and the spinal cord, suggesting that these regions receive TIP39-containing fibers from the medial paralemniscal nucleus, and unilateral lesions demonstrated that the projections are ipsilateral. The projections of the TIP39-containing cells in the subparafascicular area suggest their involvement in limbic and endocrine functions, while the projections of the TIP39-containing cells in the medial paralemniscal nucleus suggest their involvement in auditory and nociceptive functions.

Brain structures mediating the suckling stimulus-induced release of prolactin.

Suckling-induced prolactin release is a widely studied neuroendocrine reflex, comprising a neural afferent and a humoral efferent component. The information on the brain structures involved in this reflex is fairly limited. The present studies focused on this question. The following hypothalamic interventions were made in lactating rats and the dams were tested for the suckling-induced prolactin response: (i) unilateral or (ii) bilateral frontal cuts at the level of the anterior and posterior hypothalamus; (iii) administration of 5,7-dihydroxytryptamine or (iv) 6-hydroxydopamine into the hypothalamic paraventricular nucleus (PVN) to destroy serotonergic and catecholaminergic innervation of the cell group, respectively; (v) lesion of the medial subdivision of the PVN; and (vi) horizontal knife cuts below the PVN. Bilateral posterior and bilateral or unilateral anterior frontal cuts caused blockade of the suckling-induced release of prolactin. Likewise, most dams receiving 5,7-dihydroxytryptamine in the PVN did not respond to the suckling stimulus. Immunocytochemistry revealed that, in those rats which did not show a rise in plasma prolactin, there were almost no serotonergic fibres and terminals in the PVN, while in dams which exhibited a response, numerous serotonergic elements were evident. 6-Hydroxydopamine treatment did not cause significant alteration in the prolactin response. Lesion of the medial, largely parvocellular subdivision of the PVN, or horizontal knife cuts below this cell group, blocked the hormone response. The findings demonstrate for the first time that: (i) interruption of the connections between the brain stem and the hypothalamus interferes with the prolactin response to the suckling stimulus; (ii) serotonergic fibres terminating in the hypothalamic PVN are involved in the mediation of the suckling stimulus; and (iii) within the PVN, neurones in the medial, largely parvocellular subdivision of the cell group take part in the transfer of the neural signal, eventually inducing prolactin release.

Effect of neonatal treatment with monosodium glutamate on dopaminergic and L-DOPA-ergic neurons of the medial basal hypothalamus and on prolactin and MSH secretion of rats.

The effect of neonatal treatment with monosodium L-glutamate (MSG) on the dopaminergic systems of the medial basal hypothalamus has been investigated using tyrosine hydroxylase (TH) and aromatic L-amino acid decarboxylase (AADC) immunocytochemistry. Changes in plasma levels of prolactin (PRL) and alpha-melanocyte-stimulating hormone (MSH) have also been determined in intact and in MSG-treated rats after inhibition of TH by alpha-methyl-p-tyrosine (alpha-MpT) or without inhibition of enzyme activity. Monosodium glutamate resulted in a 40% reduction in the number of TH immunopositive tuberoinfundibular neurons, but no change in the number of AADC-positive tuberoinfundibular nerve cells, indicating that this reduction has occurred mainly in TH-positive but AADC-negative elements, i.e., in L-DOPA-ergic neurons. In contrast, MSG did not cause changes in the number of TH and AADC immunoreactive neurons of the periventriculohypophysial and tuberohypophysial dopaminergic systems, and it did not influence basal plasma PRL levels. alpha-methyl-p-tyrosine has increased plasma PRL concentrations in both control and MSG-treated rats of both sexes, but significantly higher responses were detected in females. None of the treatments had any effect on plasma MSH level. These findings suggest that MSG affects primarily L-DOPA-ergic neurons located in the ventrolateral part of the arcuate nucleus, but not dopaminergic neurons situated in the dorsomedial part of the arcuate nucleus; neither PRL nor MSH secretion is altered by MSG; a significant sex difference exists in the pituitary PRL response to inhibition of TH, and this response is not affected by MSG.

[Suckling-induced changes in oxytocin and alpha-melanocyte-stimulating hormone contents of the median eminence and various lobes of the pituitary gland]. / Az alpha-melanocyta-stimuláló hormon és oxytocin elválasztásának és lokális transzportjának vizsgálata szopási inger hatására a hypophysis különbözó régióiban és az eminencia medianaban.

Previous reports have implicated that pituitary-derived prolactin (PRL) is secreted from two distinct zones of mammotropes within the anterior lobe (AL). The inner zone (AL-IZ), located adjacent to the NIL, is supposed to be involved in the rapid and massive discharge of PRL from the pituitary gland due to suckling stimulus. Anatomically, the AL-IZ has an intimate contact with the NIL because the blood arriving from the posterior pituitary through the short portal vessels (SPV) baths it first. Based on these facts it would be hypothesized that the locally released and/or produced important compounds, like oxytocin (OXT) and alpha-melanocyte-stimulating hormone (alpha-MSH), can be delivered to the AL-IZ. Therefore, the purpose of this study was to examine the possible local transportation of these hormones into various regions of the pituitary gland (adenohypophysis inner-zone (AL-IZ), outer zone (AL-OZ), intermediate lobe (IL), neural lobe (NL)) and median eminence of lactating rats. We have measured the concentration of OXT and alpha-MSH from tissue samples of nonsuckled and suckled rats using specific RIA-s. There were no changes in the concentration of OXY and alpha-MSH in the AL-IZ and AL-OZ due to suckling stimulus. In contrast, our data provide compelling evidence that OXT is transported into the IL, which can be further increased by suckling stimulus. Our data have shown a lack of local delivery of either alpha-MSH or OXY into the AL that raises serious doubt about their possible role in PRL secretion during suckling stimulus.

[Biosynthesis of the antibiotic gramicidin S by a Bacillus brevis culture associated with a change in growth kinetics]. / Biosintez antibiotika gramitsidina S kul'turoi Bacillus brevis v sviazi s izmeneniem kinetiki rosta.

The effect of changes in the kinetics of growth on gramicidin S biosynthesis by Bacillus brevis var. G.-B. was studied. The synthesis of gramicidin S is induced when the specific growth rate decreases, whatever is the factor causing this decrease. As was found experimentally, only cells of a certain age can synthesize gramicidin S.

[Growth limitations and biosynthesis of gramicidin in Bacillus brevis var. G.-B]. / Limitatsiia rosta i biosintez gramitsidina s Bacillus brevis var. G.-B.

Gramicidin S biosynthesis was studied in Bacillus brevis var. G.-B. during its batch and continuous cultivation when the culture growth was limited with nutrient sources (glycerol, ammonium nitrogen, phosphate), oxygen deficiency and the action of a physical factor (a low temperature). The antibiotic biosynthesis was shown to be induced by a change in the growth rate caused by the action of any factor decelerating the growth. The authors propose a mathematical model for the antibiotic synthesis, biomass accumulation and the utilization of a substrate limiting the growth. The model is based on the age separation of cells. The model is analyzed in terms of optimizing the one-stage continuous cultivation process. The model allows one to calculate optimal conditions of the antibiotic synthesis in the process of one-stage continuous cultivation.