scholarly journals RAPD Profiling, DNA Fragmentation, and Histomorphometric Examination in Brains of Wistar Rats Exposed to Indoor 2.5 Ghz Wi-Fi Devices Radiation

2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
A. O. Ibitayo ◽  
O. B. Afolabi ◽  
A. J. Akinyemi ◽  
T. I. Ojiezeh ◽  
K. O. Adekoya ◽  
...  
Keyword(s):  
Young Male ◽  
High Technology ◽  
Male Rats ◽  
Free Access ◽  
Agarose Gel Electrophoresis ◽  
Vascular Congestion ◽  
Access To Food ◽  
The Brain ◽  
Group 1 ◽  
Brain Tissues

The advent of Wi-Fi connected high technology devices in executing day-to-day activities is fast evolving especially in developing countries of the world and hence the need to assess its safety among others. The present study was conducted to investigate the injurious effect of radiofrequency emissions from installed Wi-Fi devices in brains of young male rats. Animals were divided into four equal groups; group 1 served as control while groups 2, 3, and 4 were exposed to 2.5 Ghz at intervals of 30, 45, and 60 consecutive days with free access to food and water ad libitum. Alterations in harvested brain tissues were confirmed by histopathological analyses which showed vascular congestion and DNA damage in the brain was assayed using agarose gel electrophoresis. Histomorphometry analyses of their brain tissues showed perivascular congestion and tissue damage as well.

An orexigenic role for μ-opioid receptors in the lateral parabrachial nucleus

2003 ◽  
Vol 285 (5) ◽  
pp. R1055-R1065 ◽  
Author(s):  
John D. Wilson ◽  
Danielle M. Nicklous ◽  
Vincent J. Aloyo ◽  
Kenny J. Simansky
Keyword(s):  
Food Intake ◽  
Male Rats ◽  
Parabrachial Nucleus ◽  
Opioid Antagonist ◽  
Free Access ◽  
Lateral Parabrachial Nucleus ◽  
Μ Opioid Receptor ◽  
Access To Food ◽  
The Brain ◽  
Μ Opioid Receptors

The pontine parabrachial nucleus (PBN) has been implicated in regulating ingestion and contains opioids that promote feeding elsewhere in the brain. We tested the actions of the selective μ-opioid receptor (μ-OR) agonist [d-Ala2,N-Me-Phe4,Gly5-ol]enkephalin (DAMGO) in the PBN on feeding in male rats with free access to food. Infusing DAMGO (0.5-4.0 nmol/0.5 μl) into the lateral parabrachial region (LPBN) increased food intake. The hyperphagic effect was anatomically specific to infusions within the LPBN, dose and time related, and selective for ingestion of chow compared with (nonnutritive) kaolin. The nonselective opioid antagonist naloxone (0.1-10.0 nmol intra-PBN) antagonized DAMGO-induced feeding, with complete blockade by 1.0 nmol and no effect on baseline. The highly selective μ-opioid antagonist d-Phe-Cys-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP; 1.0 nmol) also prevented this action of DAMGO, but the κ-antagonist nor-binaltorphimine did not. Naloxone and CTAP (10.0 nmol) decreased intake during scheduled feeding. Thus stimulating μ-ORs in the LPBN increases feeding, whereas antagonizing these sites inhibits feeding. Together, our results implicate μ-ORs in the LPBN in the normal regulation of food intake.

Changes in body composition attendant on force feeding

1959 ◽  
Vol 196 (5) ◽  
pp. 965-968 ◽  
Author(s):  
Clarence Cohn ◽  
Dorothy Joseph
Keyword(s):  
Body Weight ◽  
Metabolic Pathways ◽  
Male Rats ◽  
Free Access ◽  
Carbohydrate Diet ◽  
Experimental Animals ◽  
Force Feeding ◽  
Feeding Regimen ◽  
Ad Libitum ◽  
Access To Food

Normal young adult male rats were either force-fed or allowed to eat ad libitum a moderate carbohydrate diet for 3–4 weeks. The force-fed animals were given either the amount of diet consumed by the animals eating ad libitum (pair-fed) or 80% of this amount (underfed). After a 2-week period of observation, we found that the rats eating ad libitum gained 65 gm of body weight, the pair-fed, force-fed 62 gm and the underfed, force-fed 40 gm. On the basis of the water, fat and protein content of the skin, viscera and carcass of control animals killed at the beginning of the feeding regimen and of similar constituents of the experimental animals after 2 weeks of feeding, the composition of the newly formed tissues of the various groups of animals consisted of the following: a) the rat with free access to food—water = 67.8%, fat = 7.8% and protein = 22.4%; b) the pair-fed, force-fed animal—water = 55.5%, fat = 23.6% and protein = 17.7%; c) the underfed, force-fed animal—water = 64.4%, fat = 7.9% and protein = 20.0%. The ratio of calories retained in newly formed tissue to the calories ingested over the 2-week period was 11.9% for the animals eating ad libitum, 20.6% for the pair-fed, force-fed animals and 9.5% for the underfed, force-fed rats. Force feeding appears to change intermediary metabolic pathways in the direction of increased ‘efficiency’ with resultant greater fat deposition.

scholarly journals ПОВЕДІНКОВА АКТИВНІСТЬ ЩУРІВ І РІВЕНЬ ЕНДОТОКСИКОЗУ МОЗКУ НА ТЛІ ГІДРАЗИНОВОГО ГЕПАТИТУ

2019 ◽  
Vol 76 (2) ◽  
pp. 78-84
Author(s):  
O. A. Makarenko ◽  
T. V. Hladkyi ◽  
A. V. Maikova ◽  
T. V. Mohylevska
Keyword(s):  
Open Field ◽  
Urease Activity ◽  
Toxic Hepatitis ◽  
Male Rats ◽  
Behavioural Activity ◽  
Animal Physiology ◽  
Malondialdehyde Content ◽  
Experimental Formation ◽  
The Brain ◽  
Brain Tissues

Hepatic encephalopathy is a frequent complication and manifestation of liver diseases, and a consequence of liver failure. Our research aims at studying behavioral and emotional activity, as well as identification of the degree of endotoxicosis of brain tissues of rats at the background of modelling in them of toxic chronic hydrazine hepatitis. The research was carried out at the Department of Human and Animal Physiology of Odessa National Mechnykov University on laboratory male rats, aged 8-10 months. The animals were divided into 2 groups, 6 animals in each, control (intact animals) and experimental (formation of a model of toxic hydrazine hepatitis) ones. The functional state of the brain of rats was evaluated by studying the behavioral and emotional activities of animals with the methods of "Open field" and "T- shaped labyrinth". In brain homogenates, the activity of a number of enzymes was determined, which could indicate the cause of changes in the functioning of the nervous system: the activity of lysozyme, urease, elastase, catalase, the content of malondialdehyde. It was discovered that formation of toxic hepatitis in rats is accompanied by inhibition of orientation and behavioural activity – on 50-70 %, exploratory – on 40-60 % and emotional – on 30 % in “open field” test, considerable aggravation of dynamics of rate and quality of learning problem solving in T-shaped labyrinth. Modeling of hepatitis in rats led to the decrease in lysozyme activity by 22.1%, catalase activity by 30.8%, detection of urease activity in the brain, as well as an increase in elastase activity by 44.6% and malondialdehyde content by 21.5%.в At the background of hepatitis in homogenates of brain tissues urease activity has been detected, activity of inflammation markers and enzymes-destructors increases, with activity of indices of antioxidant brain system decreasing. Change of behavioural activity of rats at the background of toxic hepatitis is caused by the development of endotoxicosis, which results from impairment of the function of liver detoxification.

scholarly journals The role of dietary niacin intake and the adenosine-5′-diphosphate-ribosyl cyclase enzyme CD38 in spatial learning ability: is cyclic adenosine diphosphate ribose the link between diet and behaviour?

2008 ◽  
Vol 21 (1) ◽  
pp. 42-55 ◽  
Author(s):  
Genevieve S. Young ◽  
James B. Kirkland
Keyword(s):  
Spatial Learning ◽  
Young Male ◽  
Adenosine Diphosphate ◽  
Pyridine Nucleotide ◽  
Learning Ability ◽  
Learning Performance ◽  
Male Rats ◽  
Current Evidence ◽  
Niacin Deficiency ◽  
The Brain

The pyridine nucleotide NAD+is derived from dietary niacin and serves as the substrate for the synthesis of cyclic ADP-ribose (cADPR), an intracellular Ca signalling molecule that plays an important role in synaptic plasticity in the hippocampus, a region of the brain involved in spatial learning. cADPR is formed in part via the activity of the ADP-ribosyl cyclase enzyme CD38, which is widespread throughout the brain. In the present review, current evidence of the relationship between dietary niacin and behaviour is presented following investigations of the effect of niacin deficiency, pharmacological nicotinamide supplementation and CD38 gene deletion on brain nucleotides and spatial learning ability in mice and rats. In young male rats, both niacin deficiency and nicotinamide supplementation significantly altered brain NAD+and cADPR, both of which were inversely correlated with spatial learning ability. These results were consistent across three different models of niacin deficiency (pair feeding, partially restricted feeding and niacin recovery). Similar changes in spatial learning ability were observed inCd38− / − mice, which also showed decreases in brain cADPR. These findings suggest an inverse relationship between spatial learning ability, dietary niacin intake and cADPR, although a direct link between cADPR and spatial learning ability is still missing. Dietary niacin may therefore play a role in the molecular events regulating learning performance, and further investigations of niacin intake, CD38 and cADPR may help identify potential molecular targets for clinical intervention to enhance learning and prevent or reverse cognitive decline.

N-(3,5-dinitrophenyl)-5-methoxytryptamine, a novel melatonin antagonist: effects on sexual maturation of the male and female rat and on oestrous cycles of the female rat

1988 ◽  
Vol 116 (1) ◽  
pp. 43-53 ◽  
Author(s):  
M. Laudon ◽  
Z. Yaron ◽  
N. Zisapel
Keyword(s):  
Drinking Water ◽  
Adult Female ◽  
Sexual Maturation ◽  
Young Male ◽  
Female Rats ◽  
Male Rats ◽  
Female Rat ◽  
Simultaneous Administration ◽  
Serum Concentrations ◽  
The Brain

ABSTRACT N-(3,5-dinitrophenyl)-5-methoxytryptamine (ML-23) has recently been synthesized and shown to antagonize the inhibitory effect of melatonin on the release of dopamine in vitro from the hypothalamus of female rats. In the present study the ability of ML-23 to inhibit in vivo the following melatonin-mediated effects was investigated: (1) delayed sexual maturation of young male rats, (2) delayed sexual maturation of young female rats, (3) inhibition of ovulation in mature female rats and (4) re-establishment of oestrous cycles in adult female rats maintained in continuous light. The inhibitory effect of daily melatonin injections, given in the afternoon, on the growth of the prostate gland and seminal vesicles and on serum testosterone concentrations in young male rats was prevented by daily injections of ML-23. Daily injections of ML-23 alone did not affect sexual maturation of young rats. In young male rats treated through the drinking water with melatonin, the growth of the accessory sex organs, but not that of the testes, was delayed and serum concentrations of testosterone were lower than in untreated rats. Administration of ML-23 through the drinking water increased serum concentrations of testosterone but did not significantly affect the weights of the accessory sex organs. Simultaneous administration of ML-23 and melatonin through the drinking water prevented completely, in a dose-dependent manner, the melatonin-mediated decrease in epididymal weights and in serum concentrations of testosterone and partially inhibited the delayed growth of the prostate glands and seminal vesicles. In young female rats treated with melatonin through the drinking water for 30 days, the growth of the ovaries was inhibited and serum concentrations of oestradiol were lower than in untreated rats. The growth of the uterus was not significantly affected. Administration of ML-23 through the drinking water did not significantly affect uterine and ovarian weights or oestradiol concentrations. Simultaneous administration of melatonin and ML-23 through the drinking water prevented completely the melatonin-mediated decrease in ovarian weights and in serum oestradiol concentrations. Ovulation during presumptive oestrus was prevented in adult female rats treated through the drinking water for 7 days with melatonin. Administration of ML-23 alone did not significantly affect the average numbers of ova shed and corpora lutea present. Simultaneous administration of ML-23 and melatonin prevented completely the melatonin-mediated inhibition of ovulation; the average number of ova shed was the same as in controls. Suppression of reproductive cycles occurred in adult female rats after long-term exposure to continuous light. This suppression was prevented by daily injections of melatonin in the afternoon; the incidence of constant oestrus decreased by 80%. Simultaneous injection of ML-23 and melatonin into rats maintained under continuous illumination prevented the effect of melatonin, and all the animals remained in constant oestrus. Administration of ML-23 alone did not alter the incidence of constant oestrus. A tritium-labelled derivative of ML-23 was prepared and administered orally to male rats. Peak concentrations of ML-23 occurred in the blood within 30 min after feeding and disappeared subsequently with a half-life of about 42 min. Intraperitoneal injection of [3H]ML-23 resulted in the appearance of peak concentrations of the drug in the brain within 20 min. The effects of ML-23 on serotonin S1 and S2 receptors, dopamine D2 receptors and melatonin receptors in the brain of the male rat were investigated using [3H]serotonin, [3H]spiperone and 2-[125I]iodomelatonin respectively. The binding of [3H]serotonin to brain synaptosomes and of [3H]spiperone to synaptosomes prepared from the cortical and caudate regions of the cerebrum was unaffected by ML-23 (10 μmol/l), whereas the binding of 2-[125I]iodomelatonin to brain synaptosomes was entirely inhibited. The results demonstrate the potency of ML-23 in antagonizing melatonin-mediated effects in the male and female rat in vivo. The drug may be administered to the animals simply through the drinking water, for relatively long periods without apparent deleterious effects on survival and welfare. ML-23 is accessible to both central and peripheral sites and acts specifically on melatonin but not on serotonin or dopamine receptors in the brain. The availability of a melatonin antagonist offers new opportunities for exploring the physiological role of melatonin in the neuroendocrine system. J. Endocr. (1988) 116, 43–53

scholarly journals Evaluation of Mutagenic and Antimutagenic Activity of Methanol Extract of Cousinia thomsonii against Cyclophosphamide

2020 ◽  
pp. 53-57
Author(s):  
Ishfaq Shafi Khan ◽  
Khalid Bashir ◽  
Naveed Gulzar ◽  
Yaseen Maqbool Bhat
Keyword(s):  
Bone Marrow Cells ◽  
Positive Control ◽  
Negative Control ◽  
Male Rats ◽  
Free Access ◽  
Antimutagenic Activity ◽  
Male Wistar Rats ◽  
Group 5 ◽  
Group 2 ◽  
Group 1

The present study was conducted to evaluate the mutagenic and antimutagenic potential of Cousinia thomsonii (CT) extract in bone marrow cells of male wistar rats using some important parameters like micronucleated polychromatic erythrocyte (MnPCE), mitotic index (MI), chromosomal aberrations (CA) and polychromatic erythrocyte to normochromatic erythrocyte ratio (PCE/NCE). 30 male rats of wistar strain were divided into 6 groups with 5 rats each group. Group 1 rats were taken as negative control having free access to distilled water and rat feed. Group 2 rats were taken as positive control treated with mutagen cyclophosphamide (CP) at dose of 60 mg/kg b wt. for 2 days. Group 3 and 4 were treated with CT extract at dose of 100 and 200 mg/kg b wt. for 20 days. Group 5 and 6 were treated with 100 and 200 mg/kg b wt of CT extract for first 18 days and for last 2 days with CP at dose concentration of 60 mg/kg. It was found that rats treated with CT extract alone did not produce any significant changes in MnPCE, PCE/NCE ratio, CA and MI when compared with control treated rats (group 1). However in group 5 and 6 rats treated with CT extract in combination with CP a protective effect was observed against the cyclophosphamide induced cellular mutagenicity. In concluding remark Cousinia thomsonii was found to show antigenotoxic potential and also produce protective antimutagenic effects against CP induced chromosomal damage.

PHOSPHORUS METABOLISM IN COLD-EXPOSED RATS

1963 ◽  
Vol 41 (11) ◽  
pp. 2209-2214 ◽  
Author(s):  
John R. Beaton
Keyword(s):  
Urinary Excretion ◽  
Cold Exposure ◽  
Inorganic Phosphorus ◽  
Male Rats ◽  
Free Access ◽  
Lipid Phosphorus ◽  
Blood Concentrations ◽  
Adenosine Phosphates ◽  
Access To Food ◽  
Phosphorus Levels

Male rats weighing 207 ± 2.38 g were exposed to cold (2–3 °C) for a period of 7 days during which urine and faeces were collected daily and analyzed for phosphorus. As a consequence of cold exposure, urinary excretion of phosphorus is increased. With free access to food, the increased food (and hence phosphorus) intake of the animals compensates for the increased urinary excretion and a normal phosphorus balance results. Cold exposure was without significant effect upon blood concentrations of acid-soluble, inorganic, organic, or lipid phosphorus. Increased inorganic and decreased organic, non-lipid phosphorus levels were observed in livers of cold-exposed rats. These observations suggest the breakdown of organic phosphates (e.g. hexose and triose phosphates, adenosine phosphates, phosphocreatine) to inorganic phosphorus.

PHOSPHORUS METABOLISM IN COLD-EXPOSED RATS

1963 ◽  
Vol 41 (1) ◽  
pp. 2209-2214
Author(s):  
John R. Beaton
Keyword(s):  
Urinary Excretion ◽  
Cold Exposure ◽  
Inorganic Phosphorus ◽  
Male Rats ◽  
Free Access ◽  
Lipid Phosphorus ◽  
Blood Concentrations ◽  
Adenosine Phosphates ◽  
Access To Food ◽  
Phosphorus Levels

Male rats weighing 207 ± 2.38 g were exposed to cold (2–3 °C) for a period of 7 days during which urine and faeces were collected daily and analyzed for phosphorus. As a consequence of cold exposure, urinary excretion of phosphorus is increased. With free access to food, the increased food (and hence phosphorus) intake of the animals compensates for the increased urinary excretion and a normal phosphorus balance results. Cold exposure was without significant effect upon blood concentrations of acid-soluble, inorganic, organic, or lipid phosphorus. Increased inorganic and decreased organic, non-lipid phosphorus levels were observed in livers of cold-exposed rats. These observations suggest the breakdown of organic phosphates (e.g. hexose and triose phosphates, adenosine phosphates, phosphocreatine) to inorganic phosphorus.

scholarly journals Reduced Muscle Glycogen Differentially Affects Exercise Performance and Muscle Fatigue

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Jay H. Williams ◽  
Timothy W. Batts ◽  
Simon Lees
Keyword(s):  
Muscle Fatigue ◽  
Muscle Glycogen ◽  
Exercise Performance ◽  
Central Fatigue ◽  
Voluntary Exercise ◽  
Male Rats ◽  
Control Group ◽  
Free Access ◽  
Lower Blood ◽  
Access To Food

This investigation examined the effects of reduced muscle glycogen on exercise performance and muscle fatigue. Male rats were assigned to a low glycogen group (LG) that participated in a protocol of exercise and fasting, a high glycogen group (HG) that exercised but were allowed free access to food, or control group (CON) that did not exercise but were allowed free access to food. Following the protocol, muscle glycogen content of the LG animals was reduced by 45%. The LG animals also performed 79 and 81% less voluntary treadmill exercise than the HG and CON groups. At exhaustion, the LG group had lower blood glucose than HG and CON but exhibited no reduction in sarcoplasmic reticulum (SR) function. During 30 min of in situ stimulation, the rates and magnitudes of muscle fatigue were not significantly different between groups, and fatigue-induced reductions in SR function were similar between groups. The results indicate that reduced muscle glycogen markedly impairs voluntary exercise performance but does not appreciably affect isolated muscle function. It is likely that exercise exhaustion due to reduced muscle glycogen is due, in large part, to hypoglycemia and central fatigue as opposed to peripheral mechanisms.

scholarly journals Eryngium Bungei Boiss Extract Has Hepatoprotective Effect Against Liver Damage Induced by Acetaminophen in Rats: Novel Antioxidant and Anti-Inflammatory Effects

2019 ◽  
Vol 13 (4) ◽  
pp. 11-16
Author(s):  
Maryam Fatemi ◽  
◽  
Tahoora Shomali ◽  
Saeed Nazifi ◽  
Mehdi Fazeli ◽  
...  
Keyword(s):  
Radical Scavenging ◽  
Male Rats ◽  
Free Access ◽  
Sod Activity ◽  
Tnf Α ◽  
Hepatoprotective Effects ◽  
Anti Inflammatory ◽  
Group 2 ◽  
Negative Controls ◽  
Group 1

Background: Acetaminophen-induced toxicity is a common cause of acute liver failure. This study investigated the hepatoprotective effects of Eryngium bungei Boiss (EB) extract against the hepatotoxicity in rats. Methods: Thirty adult male rats were randomly assigned to five groups, with free access to water and food. They were treated as follows: Group 1 (negative controls): distilled water (DW); Group 2 (positive controls): DW for 7 days and a single dose of 500 mg/kg BW acetaminophen orally on day 8th; Groups 3, 4 and 5 (experimental groups): received EB extract mixed in DW at 100, 200 and 400 mg/kg/day orally for 7 days plus 500 mg/kg acetaminophen on the 8th day. On the 9thday, blood and liver samples were collected from all rats. Results: The EB extract improved the adverse histological changes in the rats’ livers and resulted in reduced serum ALT and ALP enzymes. Oxidative stress was noted in the liver tissue in Group 2. Pretreatment with EB extract reduced MDA concentration and increased GSH levels, compared to that for Group 2. The extract at 200 and 400 mg/kg/day significantly increased SOD activity, compared to that for Group 2. The IL-1β and TNF-α levels increased significantly in Group 2, compared to those in Group 1. Administration of EB extract in Groups 3, 4 and 5 significantly decreased the IL-1β and TNF-α parameters. Conclusions: The hepatoprotective effects of EB extract appears to be linked to its glutathione-mediated detoxification, free radical scavenging and anti-inflammatory properties.

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