Tissues Of Adult Male Rats Research Articles

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Glyphosate is used as an herbicide in agriculture. At sub-agriculture concentrations, glyphosate-based herbicide inhibits cell proliferation. Glyphosate is a chelating agent that interferes with the metabolic activities in plants thereby adversely affecting its metabolism. The study aimed to determine the glyphosate-induced detrimental changes in SREBP-1c and PPAR-γ mRNA expression in adipose tissue of adult male rats. Adult male Wistar albino rats were divided into 4 groups, each consisting of 6 animals. Group I served as normal control rats; Group II-IV consisted of rats exposed to glyphosate at different concentrations (50, 100, and 250 mg/kg body weight respectively) orally for 16 weeks. After 16 weeks of treatment, the animals were sacrificed, and adipose tissue was dissected out for the assessment of SREBP-1c and PPAR-γ mRNA by real-time PCR using gene-specific down-regulated primers. The results with the p<0.05 level were considered to be statistically significant. The results showed a significant dose-dependent increase (P <0.05) in the expression of SREBP-1c in all the glyphosate-exposed rats compared to control rats and PPAR-γ mRNA expression was found to be significantly reduced in a concentration-dependent manner (P<0.05) compared to normal control animals. The current findings for the first time report that glyphosate had detrimental changes in the expression of transcription factors such as SREBP-1c and PPAR-γ mRNA in adipose tissue and thereby glyphosate may lead to the development of type-2 diabetes or insulin resistance.

DISTINCT CARDIAC CONNEXIN-43 EXPRESSION IN HEMODYNAMICALLY UPLOADED AND UNLOADED HEART MAY IMPACT VULNERABILITY TO MALIGNANT ARRHYTHMIAS

Objective: Experimental and clinical studies suggest that myocardial hypertrophy in response to hypertension and hyperthyroidism increases propensity to cardiac arrhythmias. While these are rare in conditions resulting in myocardial atrophy, such as hypothyroidism or type-1 diabetes mellitus (T1DM). One of the crucial factors impacting the susceptibility of the heart to life-threatening arrhythmias is gap junction channel protein connexin-43 (Cx43), which ensure cardiac cell-to-cell coupling for electrical signal propagation that induce contraction. We aimed to explore abundance of Cx43 protein and its cardiomyocyte topology in hemodynamically uploaded hypertrophied versus unloaded hypotrophic cardiac phenotype. Design and method: Analysis were performed in left ventricular tissue of adult male rats of following groups: 1. spontaneously hypertensive rat (SHR); 2. normotensive Wistar Kyoto rats (WKY) treated for 8-weeks with L-thyroxine (0.15 μg/kg, i.v.) to induce hyperthyroid status; 3. WKY rats treated with methimazol (0.05% solution, p.o.) to induce hypothyroid status; 4. WKY rats treated with strepotozotocin (50mg/kg, i.p.) to induce T1DM. Animals were compared with non-treated normotensive control rats. Results: Comparing to healthy non-treated rats there was a decrease of total myocardial Cx43 protein and its variant phosphorylated at serine368 in SHR and hyperthyroid rats. Besides, enhanced abnormal localisation of Cx43 was demonstrated on lateral sides of hypertrophied cardiomyocytes. In contrast, total Cx43 protein and its serine368 variant were increased in atrophied left ventricle of hypothyroid and T1DM rats. It was associated with less pronounced alterations in Cx43 topology. In parallel, the abundance of PKC epsilon, which phosphorylates Cx43 at serine368 that stabilize Cx43 function and distribution was reduced in hypertrophied heart while enhanced in atrophied once. Conclusions: Findings suggest that differences in the abundance of cardiac Cx43, its variant phosphorylated at serine368 and Cx43 topology may explain, in part, distinct propensity of uploaded and unloaded heart to malignant arrhythmias. It suggests that hemodynamically overloaded heart might benefit from interventions promoting unloading. This research was supported by VEGA grants 2/0002/20, 2/0006/23, Slovak Research and Development Agency under the Contract no. 21-0410

Palliative Effect of Resveratrol against Nanosized Iron Oxide-Induced Oxidative Stress and Steroidogenesis-Related Genes Dysregulation in Testicular Tissue of Adult Male Rats

The nano-sized iron oxide (Fe2O3-NPs) is one of the most used engineered nanomaterials worldwide. This study investigated the efficacy of natural polyphenol resveratrol (RSV) (20 mg/kg b.wt, orally once daily) to alleviate the impaired sperm quality and testicular injury resulting from Fe2O3-NPs exposure (3.5 or 7 mg/kg b.wt, intraperitoneally once a week) for eight weeks. Spermiograms, sexual hormonal levels, oxidative stress indicators, and lipid peroxidation biomarker were assessed. Moreover, the steroidogenesis-related genes mRNA expressions were evaluated. The results showed that RSV substantially rescued Fe2O3-NPs-mediated sperm defects. Additionally, the Fe2O3-NPs-induced depressing effects on sperm motility and viability were markedly counteracted by RSV. Moreover, RSV significantly restored Fe2O3-NPs-induced depletion of testosterone, follicle-stimulated hormone, luteinizing hormone, and testicular antioxidant enzymes but reduced malondialdehyde content. Furthermore, the Fe2O3-NPs-induced downregulation of steroidogenesis-related genes (3 β-HSD, 17 β-HSD, and Nr5A1) was significantly counteracted in the testicular tissue of RSV-treated rats. These findings concluded that RSV could limit the Fe2O3-NPs-induced reduced sperm quality and testicular injury most likely via their antioxidant activity and steroidogenesis-related gene expression modulation.

Effects of resistance training, palm pollen grain extracts, and testosterone injection on luteinizing hormone receptors, claudin-1, cingulin, and zonula occludens in the prostate tissues of adult male rats.

The present study aimed to investigate the effects of resistance training, Phoenix dactylifera extract, and testosterone enanthate injection on luteinizing hormone receptor, claudin-1, cingulin, and zonula occludens in the prostate tissues of adult rats. 30male rats were divided into six groups: (1) control, (2) resistance training, (3) Phoenix dactylifera extract, (4) testosterone enanthate, (5) resistance training+Phoenix dactylifera extract, and (6) resistance training+testosterone enanthate. After completing the treatments and resistance training, all rats were sacrificed via anaesthesia. The results showed that resistance training, Phoenix dactylifera, and testosterone enanthate significantly increased the luteinizing hormone receptor, claudin-1, cingulin, and zonula occludens gene expression levels in the prostate. The resistance training treatment, along with Phoenix dactylifera+testosterone enanthate, exerted synergic effects on the prostate luteinizing hormone receptor levels and claudin-1gene expression. In conclusion, Phoenix dactylifera, as a natural compound with fewer side effects than testosterone injection, can be used to enhance athletic performance. Besides, considering the potential benefits of Phoenix dactylifera, it can be considered in the treatment of testosterone deficiency; however, furtherresearch is needed.

Arabic gum ameliorates histological and histochemical changes in the renal cortex of rats induced by alloxan injection

Arabic gum (AG) is a natural branched-chain multifunctional hydrocolloid with a highly neutral or slightly acidic, arabinogalactan protein complex containing calcium, magnesium, and potassium. Arabic gum is a dried exudate obtained from the stem and branches of Acacia trees. AG has an anti-inflammatory and antioxidant effect. This study aimed to examine the possible anti-inflammatory and antioxidant effect of AG against the damage induced by alloxan injection on renal tissue of adult male rats using histological and histochemical studies. The current experiment was carried out on 48 adult male Albino rats. Rats were randomly and equally categorized into four groups 12 rats in each group as follows: 1) Control group (C): rats have left without treatment; 2) Diabetic groups (D): rats were injected with 150 mg/kg body weight of alloxan and left for 21 days ; 3) Arabic gum groups (G): rats were orally administrated (25 mg/kg body weight/day) for 21 days and 4) D+G groups: rats were injected with alloxan and treated with 25 mg/kg body weight/day for 21 days. The experimental rats were sacrificed after 7 and 21 days post-treatment. Examination of renal tissue of rats seven and twenty-one days post-alloxan injection revealed many histological and histochemical changes. Highly increased collagen fibres were demonstrated after seven and twenty-one days post alloxan injection. Also, alloxan injection significantly decreased PAS-positive materials, total protein content, and total DNA content, but it significantly increased amyloid β –protein content relative to the control group. While treatment with AG post-alloxan injection showed a trend toward lowering the incidence of renal tissue histological and histochemical changes induced by alloxan injection. According to the results obtained in the current study using AG as a natural agent showed a strong cytoprotective effect against the histological and histochemical changes due to its antioxidant effect.

Effect of Resistance Training with Palm Pollen and Testosterone on Runx2 Protein and Gene Expression Levels in Bone Tissue of Adult Male Rats

Background: A healthy lifestyle, nutrition, and exercise can improve bone mass via several mechanisms. Objectives: This study assessed the effects of four weeks of palm pollen consumption along with resistance training on protein and gene expression levels of Runt-related transcription factor 2 (Runx2) in bone tissue of rats. Methods: Thirty-six rats were selected and assigned into six groups, including (1) training + testosterone, (2) training + palm pollen, (3) testosterone, (4) palm pollen, (5) training and (6) sham. Then, 100 mg/kg of palm pollen was prescribed five days per week. Resistance training was performed five sessions per week, and 2 mg/kg of testosterone propionate was prescribed peritoneally. Gene expression and protein levels of Runx2 were measured via the real-time PCR and Western blot methods. Results: Training had a significant effect on the increase in Runx2 protein levels (P≤0.05). Training + testosterone, training + palm pollen, testosterone, and palm pollen had significant effects on gene expression and protein levels of Runx2 (P ≤ 0.05). Training + testosterone and training + palm pollen had more favorable effects on the increase of gene expression and protein levels of Runx2 than had testosterone, palm pollen, and training (P ≤ 0.05). Conclusions: Although training, palm pollen, and testosterone alone could increase the Runx2 protein levels in the bone tissue of rats, training with palm pollen and training with testosterone appeared to have more favorable effects on the increase of gene expression and protein levels of Runx2 than either alone.

Ameliorating Iron Overload in Intestinal Tissue of Adult Male Rats: Quercetin vs Deferoxamine.

Objective The aim of our study is to compare the role of the new natural alternative (Quercetin) with the current iron-chelation therapy (Deferoxamine (DFO)) in the effect of iron overload on small intestinal tissues and to investigate the possible underlying molecular mechanisms of such toxicity. Methods Forty-two adult male albino rats were divided into six groups: control groups, DFO, Quercetin, iron overload, iron overload+DFO, and iron overload+Quercetin groups. Animals received daily intraperitoneal injection of Deferoxamine (125 mg /kg), Quercetin (10 mg/kg), and ferric dextran (200 mg/kg) for 2 weeks. Results Iron overloaded group showed significant increase in serum iron, total iron binding capacity (TIBC), transferrin saturation percentage (TS %) hepcidin (HEPC), serum ferritin, nontransferrin bound iron (NTBI), and small intestinal tissues iron levels. Iron overload significantly increased the serum oxidative stress indicator (MDA) and reduced serum total antioxidant capacity (TAC). On the other hand, iron overload increased IL6 and reduced IL10 in small intestinal tissues reflecting inflammatory condition and increased caspase 3 reactivity indicating apoptosis and increased iNOs expressing cell indicting oxidative stress especially in ileum. In addition, it induced small intestinal tissues pathological alterations. The treatment with Quercetin showed nonsignificant differences as compared to treatment with DFO that chelated the serum and tissue iron and improved the oxidative stress and reduced tissue IL6 and increased IL10 and decreased caspase 3 and iNOs expressing cells in small intestinal tissues. Moreover, it ameliorated the iron overload induced pathological alterations. Conclusion Our study showed the potential role of Quercetin as iron chelator like DFO in case of iron overload induced small intestinal toxicity in adult rats because of its serum and tissue iron chelation, improvement of serum, and small intestinal oxidative stress, ameliorating iron induced intestinal inflammation, apoptosis, and histopathological alterations.

Lung injury induced by Bisphenol A: A food contaminant, is ameliorated by selenium supplementation

Bisphenol A (BPA), a widely used industrial chemical, is known to disrupt endocrine function. This study aimed to investigate the impact of chronic exposure to BPA on the lung tissue of adult male rats as well as any possible alleviating effects resulting from selenium (Se) treatment. Chronic exposure to BPA resulted in prominent inflammation and oxidative stress responses as evidenced by an increase in levels of malondialdehyde (MDA), reduced concentrations of superoxide dismutase (SOD), and upregulation of Interleukin-18 (IL-18) expression in lung tissue. In addition, chronic exposure led to modulation of the fibrosis-related gene expression, as we observed augmented follistatin-like1 (FSTL1) expression and diminished a disintegrin and metalloproteinase with thrombospondin motif 5 (ADAMTS5) expression. Se treatment remarkably mitigated changes in the expression of these dysregulated markers of lung injury. The biochemical changes were consistent with the histopathological findings, where cellular infiltration and inflammatory fibrotic changes were observed following BPA administration and a lessening of these effects with concomitant Se treatment. Taken together, the results from the study reveal that chronic exposure to BPA may promote the development of pulmonary inflammatory diseases with possible induction of lung fibrosis. Se treatment effectively suppressed oxidative stress, inflammation, and fibrosis, suggesting that Se has the potential to be used as a therapeutic agent in the treatment of pulmonary inflammatory diseases.

The effects of sleep deprivation on microRNA expression in rats submitted to pilocarpine-induced status epilepticus

Epilepsy is a neurological disorder with significant prevalence and the individuals affected by this disease have a great probability of occurrence of a lethal phenomenon known as Sudden Unexpected Death in Epilepsy (SUDEP). SUDEP occurs mainly during the night and probably during sleep. The pathophysiological mechanisms involved in this lethal phenomenon are still obscure and new evidences that could corroborate in this area are warranted. Thus, the aim of the present study was to evaluate the effect of sleep deprivation in the expression of microRNA (miRNA) in the frontal cortex and heart tissues of adult male rats after 50days of saline (SAL) or pilocarpine-induced status epilepticus (PILO). Initially 389 miRNA expressions were evaluated between SAL and PILO groups by microarray. Subsequently, 3 differentially expressed miRNAs of each tissue were investigated after total sleep deprivation (TSD 6h) and paradoxical sleep deprivation (PSD 24h). Still, it was analyzed that the effects of sleep rebound with equivalent duration of PSD and TSD. There was a significant increase of miR-146a expression, an important inflammatory modulator in the frontal cortex of PILO rats when compared to SAL animals. Animals treated with pilocarpine were affected by TSD (through overexpression of miRNAs related to inflammatory process) and these changes were maintained even after a sleep window of 6h. In contrast, miRNAs associated with heart diseases were down-regulated in PSD rebound, suggesting a possible restoration of homeostasis in cardiovascular system of SAL and PILO groups.

Formaldehyde exposure induces autophagy in testicular tissues of adult male rats

Formaldehyde, a ubiquitous environmental pollutant, has long been suspected of causing adverse male reproductive effects. However, the molecular and cellular mechanisms underlying this phenomenon remain elusive. The overall aim of this study is to clarify the role of autophagy in male reproductive injuries induced by formaldehyde exposure, by which we can further understand the molecular mechanism of spermatogenesis and develop new targets for prevention and treatment of male infertility. In this study, electron microscopy, Western blot, and RT-PCR analysis were used to detect autophagy in testicular tissues. Moreover, testicular weights, histopathology, and morphometry were used to evaluate the reproductive injuries of formaldehyde exposure. We found that formaldehyde exposure-induced autophagy in testicular tissues was dose dependent. Increasing autophagosomes in spermatogenetic cells was observed by electron microscopy in formaldehyde exposure group. In addition, RT-PCR and Western blot analysis showed the transcription levels of the LC3-II, as well as the conversion from LC3-I to LC3-II, an indicator of autophagy, significantly increased in testicular tissue of formaldehyde exposure group in a dose dependent manner when compared with those in control group. Furthermore, the alterations of autophage were basically consistent with the changes in testicular weight and morphologic findings. In summary, formaldehyde exposure triggered autophagy, and autophagy may be a scathing factor responsible for male reproductive impairment induced by formaldehyde.

Recombinant truncated and microsomal heme oxygenase-1 and -2: differential sensitivity to inhibitors

Recombinant truncated forms of heme oxygenase-1 and -2 (HO-1 and HO-2) were compared with their crude microsomal counterparts from brain and spleen tissue of adult male rats with respect to their inhibition by azole-based, nonporphyrin HO inhibitors. The drugs tested were an imidazole-alcohol, an imidazole-dioxolane, and a triazole-ketone. Both the recombinant and crude forms of HO-2 were similarly inhibited by the 3 drugs. The crude microsomal spleen form of HO-1 was more susceptible to inhibition than was the truncated recombinant form. This difference is attributed to the extra amino acids in the full-length enzyme. These observations may be relevant in the design of drugs as inhibitors of HO and other membrane proteins.

Testosterone deficiency impairs glucose oxidation through defective insulin and its receptor gene expression in target tissues of adult male rats

Testosterone and insulin interact in their actions on target tissues. Most of the studies that address this issue have focused on the physiological concentration of testosterone, which maintains normal insulin sensitivity but has deleterious effects on the same when the concentration of testosterone is out of this range. However, molecular basis of the action of testosterone in the early step of insulin action is not known. The present study has been designed to assess the impact of testosterone on insulin receptor gene expression and glucose oxidation in target tissues of adult male rat. Adult male albino rats were orchidectomized and supplemented with testosterone (100 μg/100 g b. wt., twice daily) for 15 days from the 11th day of post orchidectomy. On the day after the last treatment, animals were euthanized and blood was collected for the assay of plasma glucose, serum testosterone and insulin. Skeletal muscles, such as gracilis and quadriceps, liver and adipose tissue were dissected out and used for the assay of various parameters such as insulin receptor concentration, insulin receptor mRNA level and glucose oxidation. Testosterone deprivation due to orchidectomy decreased serum insulin concentration. In addition to this, insulin receptor number and its mRNA level and glucose oxidation in target tissues were significantly decreased ( p < 0.05) when compared to control. However, testosterone replacement in orchidectomized rats restored all these parameters to control level. It is concluded from this study that testosterone deficiency-induced defective glucose oxidation in skeletal muscles, liver and adipose tissue is mediated through impaired expression of insulin and its receptor gene.

Influence of Gamma Irradiation on DNA Methylation in Liver of Male Rats and their Offspring

In the present work, the influence of gamma radiation (3 Gy) on DNA methylation in slowly proliferating liver tissue of adult male rats and their offspring was studied. Total methylation of DNA was determined on the basis of presence of 5-methylcytosine at the inner cytosine of the C-C-G-G sequence by using restriction enzymes, endonuclease Msp I and its isoschisomer Hpa II. It was found that in the liver of control animals, molecular weight distribution of both Msp I and Hpa II digestion products of DNA and the level of DNA methylation were influenced by age mainly between the 3rd and the 7th days of life. At this time, significant difference was found especially in products of cleavage with enzyme Msp I, where an increase in DNA fragments of medium molecular weight (1 - 7 kb) occurred. The changes in the molecular weight distribution of DNA digestion products in the offspring of control rats were accompanied by an increase in the level of total DNA methylation from 29.8% to 67%. In the offspring of irradiated males, the level of DNA methylation was higher in comparison with the offspring of non-irradiated control males, especially on the 3rd day after birth. We suppose that this finding is conjoined with a transgeneration transfer of radiation-induced genome damage.

Detection of lead-induced oxidative stress in the rat epididymis by chemiluminescence

It has been shown that lead (Pb) is able to induce lipid peroxidation, one of the main manifestations of oxidative stress. In this study we examined the relationship between chronic Pb exposure and level of reactive oxygen species (ROS) in reproductive system tissues of sexually mature male Wistar rats. One group of animals (control, K) was allowed to drink distilled water, the second group (Pb) was allowed to drink freely 1% aqueous solution of lead acetate. Another groups had a following supplements: rats were allowed to drink distilled water containing vitamin C (vit C) at concentration of 500 mg/l or Trolox (a vitamin E analog) at concentration of 48 mg/l or vit C (500 mg/l) + Trolox (48 mg/l). The similar groups among Pb-treated animals were examined after treatment with the same vitamins and using the same vitamin doses, dissolved in 1% aqueous solution of lead acetate. In all cases the time of drinking was 6 months. It was found that lead content in samples of tissues from testis, epididymis and in a whole blood in Pb- and Pb with antioxidants treated rats was significantly elevated. Chemiluminescence (CL) emitted by the Pb-treated tissues was significantly higher when compared to the light emission by tissues isolated from the animals of control group. The increase in the CL caused by lead occurs in the following increasing order within the studied tissues: cauda of epididymis <testis< caput of epididymis (19%, 39% and 51%, respectively). Dietary vit C supplementation to the Pb-treated rats for 6 months period decreased the CL from caput of epididymis, cauda of epididymis and testis (by 43%, 24%, 39%, respectively) more effectively in comparison to the control group (35%, 17%, 33%, respectively). Also stronger quenching effect on the light emission from the above mentioned tissues after Trolox supplementation was observed in the Pb-treated group (42%, 21%, 35%, respectively) than in the control group (23%, 13%, 13% respectively). The combination of both antioxidants treatments (vit C and Trolox) did not give a higher significant quenching effect compared to the treatment with the vitamins separately. No ultrastructural changes were found in the seminiferous epithelium of Pb-treated animals. However, we found abnormalities in ultrastructure of epididymal epithelial cells and epididymal spermatozoa in rats of Pb-treated groups. These findings provide ex vivo evidence that Pb causes oxidative cellular damage in reproductive system tissues of adult male rats, which may be closely associated with the ROS production.

Expression of kininogen genes by rat cardiomyocytes

To determine the existence of the kallikrein–kinin system in the heart, we have studied in vitro and in vivo whether rat heart expresses kininogens (KGNs). The reverse transcription-polymerase chain reaction (RT-PCR) for KGN mRNAs demonstrated that the cardiac tissue of adult male rats expresses T-KGN mRNA but not high-molecular-weight (H-) KGN mRNA. An intravenous injection of lipopolysaccharide (LPS) resulted in a significant increase in T-KGN mRNA levels of rat heart within 12 h. Polyacrylamide gel electrophoresis of cDNA products generated by RT-PCR from heart mRNA using primers specific for either T- or low-molecular-weigh (L-) KGN revealed that rat heart expressed not only T-KGN gene but also L-KGN gene, and that LPS injection exclusively stimulated the expression of T-KGN but not of L-KGN gene. T-KGN mRNA was also detected in cultured myocytes derived from fetal rat heart, and the expression was markedly enhanced by an addition of LPS to cultures. These results demonstrated that rat cardiomyocytes are the source of T- and L-KGNs but not of H-KGN, and that their expression of T-KGN mRNA is stimulated by LPS, probably via LPS-receptor CD14.

Changes of hydration of rats' tissues after in vivo exposure to 0.2 Tesla steady magnetic field.

Hydration and [3H]ouabain uptake by different tissues of adult male rats were measured immediately after exposure to homogenous 0.2 T steady magnetic field. A time-dependent decrease of hydration and adaptation, followed by disadaptation, was detected in brain and liver tissues in most of the rats after 3.5-5 h of exposure. The number of functional active ouabain binding receptors, which correlates with cell volume, was also decreased in brain, liver, and spleen and increased in kidney tissue after half an hour of exposure. It is suggested that cell hydration is a second messenger through which the SMF exerts its influence.

(-)-Nicotine increases mRNA encoding G3PDH and the vesicular acetylcholine transporter in vivo.

The effects of acute in vivo (-)-nicotine exposure on neuronal expression of mRNA encoding the vesicular acetylcholine transport (VAChT) and the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (G3PDH) were examined. The reverse transcription polymerase chain reaction was used to amplify cDNA derived from brain tissue of adult male rats injected acutely with (-)-nicotine and semi-quantification of cDNA products conducted using anion exchange chromatography. In cerebral cortex, levels of cDNA derived from the VAChT mRNA were increased by > 65% above control levels 1 h after (-)-nicotine (0.8 mg/kg, s.c.) exposure. In hippocampal samples, levels of this cDNA were increased by 15% above control levels. cDNA derived from G3PDH mRNA was increased by 86% and 280% above control levels in the cerebral cortex and hippocampus, respectively. Thus, increased expression and function of proteins associated with these mRNA species are likely consequences of acute (-)-nicotine exposure.

Cellular localization of vasopressin V1a receptor messenger ribonucleic acid in adult male rat brain, pineal, and brain vasculature.

Vasopressin V1a receptor (V1aR) transcripts were localized in brain, pineal, and superficial brain vascular tissues of adult male rats using hybridization histochemistry and an [35S]riboprobe complementary to the messenger ribonucleic acid (mRNA) encoding the fifth to the midseventh transmembrane regions of the receptor. V1aR mRNA was extensively distributed throughout brain and was expressed in 1) superficial cells of the granule cell layers of the main olfactory bulb, hippocampal dentate gyrus, and cerebellum; 2) numerous anatomically distinct brain nuclei; 3) isolated cells dispersed throughout the central nervous system; 4) cells of the choroid plexus, occasional blood vessels in the olfactory bulb and interpeduncular nucleus, and extraparenchymal intracranial vasculature; and 5) some white matter structures. Numerous cells expressing V1aR transcripts were found in forebrain structures, including primary olfactory (piriform) cortex, the anterior and posterior olfactory nuclei; dorsal, intermediate, and ventral lateral septal nuclei; the septo-fimbrial nucleus and accumbens nucleus; and numerous hypothalamic regions with the most intense hypothalamic labeling in the arcuate, stigmoid, suprachiasmatic, and periventricular nuclei and the lateral hypothalamic area. Cells expressing V1aR transcripts were ubiquitous throughout the midbrain, pontine, and medullary regions. A lower intensity signal was found in cells of the parvocellular paraventricular and anteroventral nucleus of the thalamus, circumventricular organs including the pineal, and the subfornical organ. V1aR transcripts were not generally detected in parenchymal vasculature, but could be found over large blood vessels in the interpeduncular nucleus and medial olfactory bulb; transcripts were commonly detected in perivascular brain cells. V1aR mRNA was abundantly expressed by choroid plexus, endothelial cells of midline blood vessels between the main olfactory bulbs, and superficial vascular tissue on all brain surfaces. These data confirm the presence of the vascular/hepatic-type V1aR gene in brain tissue and document an extensive expression. The distribution of V1aR mRNA suggests that there are at least two types of vasopressin-responsive cells in brain: one type exemplified by lateral septal ara neurons innervated by classical axodendritic/somatic synaptic vasopressinergic terminals and a second, perivascular/vascular type that would facilitate humoral vasopressinergic signaling in the brain.

Elimination of radiolabelled recombinant human insulin-like growth factor binding protein-3 from the circulation, and its distribution amongst organs and tissues in adult male rats.

Most insulin-like growth factor-I (IGF-I) in blood is found in complex with IGF binding protein-3 (IGFBP-3). An additional association of IGFBP-3 with an acid-labile subunit is thought to severely limit its ability to cross the vascular endothelium. However, it is not clear whether IGFBP-3 which is not complexed to acid-labile subunit can gain access to tissues and contribute to the transcapillary transport of IGF-I. We have investigated the concentration time profile of 125I-labelled recombinant, non-glycosylated human IGFBP-3 in the rat circulation, its appearance within various organs, urine, and in peritoneal lavage fluid. Radiolabelled IGFBP-3 was administered as a single infusion over 1 min into the catheterized jugular vein of male Wistar rats. Blood was sampled from the femoral artery, and urine by cannulation of the bladder for up to 3 h. The peritoneal cavity was cannulated to allow for the collection of lavage fluid. In a separate series of animals various organs were collected up to 3 h following administration of 125I-labelled IGFBP-3, and the content of radiolabel estimated by gamma spectrometry. Radiolabelled IGFBP-3 was rapidly cleared from the circulation initially (half-life 25 min), however from 70 min life to 3 h the levels of radiolabel remained constant. Neutral gel filtration on Sephadex G200 revealed that 1 h following administration the majority of the [125I]IGFBP-3 existed within a complex of 100-120 kDa, likely to represent an association with the acid-labile subunit. Radioactivity was detected in urine within 30 min of IGFBP-3 administration, was maximally present at 60 min, but declined thereafter. A proportion of the radiolabel in urine represented degraded protein fragments of IGFBP-3, although only 8% of the administered radiolabel was excreted within urine over 3 h. Within 10 min of entry into blood 125I-labelled IGFBP-3 was found within peritoneal lavage fluid. Most of the radiolabel was accumulated within the kidneys, liver, stomach and intestine up to 3 h after administration. However, while the hepatic and renal content were maximal after 30 min, stomach content continued to rise over 1 h, and stabilized at 15% of administered dose for up to 3 h. The results suggest that when not in complex with the acid-labile subunit, IGFBP-3 can rapidly cross capillary endothelia from blood to extravascular compartments. While kidney and liver are likely sites of excretion and degradation, a substantial proportion of IGFBP-3 is also accumulated by gastrointestinal tissues.(ABSTRACT TRUNCATED AT 400 WORDS)

Education and Training in the Care and Use of Laboratory Animals: A Guide for Developing Institutional Programs.Committee on Educational Programs in Laboratory Animal Science, Institute of Laboratory Animal Resources, Commission on Life Sciences, National Research Council

Previous articleNext article No AccessNew Biological BooksEducation and Training in the Care and Use of Laboratory Animals: A Guide for Developing Institutional Programs. Committee on Educational Programs in Laboratory Animal Science, Institute of Laboratory Animal Resources, Commission on Life Sciences, National Research CouncilCharles C. MiddletonCharles C. Middleton Search for more articles by this author PDFPDF PLUS Add to favoritesDownload CitationTrack CitationsPermissionsReprints Share onFacebookTwitterLinkedInRedditEmail SectionsMoreDetailsFiguresReferencesCited by The Quarterly Review of Biology Volume 67, Number 1Mar., 1992 Published in association with Stony Brook University Article DOIhttps://doi.org/10.1086/417542 Views: 2Total views on this site Citations: 1Citations are reported from Crossref Copyright 1992 The University of ChicagoPDF download Crossref reports the following articles citing this article:Arwa A. El-Sheikh, Shimaa Hamed Ameen, Samaa Salah AbdEl-Fatah Ameliorating Iron Overload in Intestinal Tissue of Adult Male Rats: Quercetin vs Deferoxamine, Journal of Toxicology 2018 (Nov 2018): 1–13.https://doi.org/10.1155/2018/8023840