Non-exposed Rats Research Articles

Protective effect of vitamin E on nickel sulfate-induced renal dysfunction in rats

Introduction: The kidney is a major organ for nickel induced toxicity. Objectives: The purpose of this investigation was to determine the protective impact of vitamin E on nickel sulfate (NiSO4 ) caused kidney dysfunction in rats using biochemical and histopathological approaches. Materials and Methods: Adult male Wistar rats were selected as animal models and randomly divided into four groups (five rats in each group) as follows; group 1. The animals received orally (gavage) 250 mg/kg vitamin E (dissolved in corn oil) 30 minutes before inhalation exposure to1mg NiSO4 /m3 . This experiment was performed for 6 hours daily for 10 consecutive days. Group 2; the rats received by gavage corn oil (vehicle) 30 minutes before inhalation exposure to1mg NiSO4 /m3 . This experiment was performed for 6 hours daily for 10 consecutive days. Group 3; animals of this group were given by gavage 250 mg/kg vitamin E only (without exposure to NiSO4 ) for 10 consecutive days. Group fourth were received by gavage an equal volume of vehicle (corn oil) for 10 consecutive days. All animals were killed 24 hours after the last treatments with sodium pentobarbital. Kidney tissues were removed. One part of the tissues were used for glutathione (GSH) and malondialdehyde (MDA) determination, other parts were fixed and processed for light microscopy. Results: The levels of MDA significantly increased and GSH decreased in rats exposed to NiSO4 in comparison to those in non-exposed rats. Histopathological observations also indicated that NiSO4 induced damage in the kidney. Additionally, administration of vitamin E prior to exposure to NiSO4 markedly decreased renal damage-induced by NiSO4 . Conclusion: The study showed that respiratory inhalation of NiSO4 induced oxidative stress and caused cell damage in rats’ kidney. Vitamin E effectively alleviated Ni-induced nephrotoxicity in rats. These observations suggest that vitamin E may have a protective effect against Ni-induced oxidative stress in the rats’ kidney.

The effect of 1800 MHz radio-frequency radiation on NMDA receptor subunit NR1 expression and peroxidation in the rat brain in healthy and inflammatory states

BackgroundThe aim of this study was to evaluate the effect of repeated exposure (5 times for 15min) of 1800MHz radio-frequency radiation (RFR) on N-methyl-d-aspartate receptor subunit NR1 (NMDA-NR1) expression in the brains of rats in a persistent inflammatory state. We also measured the effect of RFR combined with tramadol (TRAM) to determine the potential antioxidant capacity of this agent. MethodsThe effects of the Global System for Mobile Communication (GSM) modulated 1800MHz RFR exposure on the expression and activity of glutamate receptor channels with antioxidative activity in brain tissue was measured using oxygen radical absorbance capacity (ORAC) and electron spin resonance (ESR) detection of the hydroxyl radical generated by the Fenton reaction. NMDA-NR1 was measured in the cerebral tissue of rats with inflammation (complete Freund’s adjuvent) and those injected with tramadol after RFR exposure (RFR, RFR/TRAM) and in non-exposed (baseline, TRAM) rats. ResultsNo differences between the baseline group and the exposed group (RFR) were observed. NMDA-NR1 expression decreased after CFA injection and RFR exposure, and an elevated expression of NMDA-NR1 was observed in healthy control rats of both groups: TRAM/RFR and RFR. ConclusionsORAC assessment revealed a robust effect of RFR, however the other experiments revealed equivocal effects. Further studies examining the combination of ORAC with NMDA are warranted to elucidate more clearly the effect of RFR on the brain.

Adrenalectomy abolishes hypergravity-induced gastric acid hyposecretion.

Jet fighter pilots experience high gravitational acceleration forces in the cephalocaudal direction (+Gz), causing severe stress. Stress affects different physiological functions of the gastrointestinal tract. Although the effects of exposure to hypergravity on cardiovascular and cerebral functions have been the subject of numerous studies, crucial information regarding potential pathophysiological alterations following hypergravity exposure in the gastrointestinal tract is lacking. We recently documented a significant decrease in gastric secretory activity in rats after acute exposure to hypergravity. In the present study, we investigated the effects of adrenalectomy on gastric acid secretion and plasma gastrin level in hypergravity-exposed rats. Male Sprague-Dawley rats were adrenalectomized and exposed to +10Gz three times for 3 min. Gastric juice and blood samples were collected, and the volume and total acidity of gastric juice and plasma level of gastrin were measured. Consistent with our previous data, acute exposure to +10Gz significantly altered the gastric juice parameters in the sham-operated rats. The volume (P < 0.001) and acidity (P < 0.001) of gastric juice in the hypergravity-exposed rats were significantly lower than those in the nonexposed rats. In contrast, in adrenalectomized rats, the differences in the gastric juice volume (P = 0.712) and acidity (P = 0.279) were not statistically significant between the hypergravity-exposed and nonexposed rats. We demonstrated that adrenalectomy abolished hypergravity-induced gastric acid hyposecretion, but did not influence gastrin release. These findings suggest that the adrenal glands are required for hypergravity-induced gastric acid hyposecretion.

Gastric acid response to acute exposure to hypergravity.

The influence of environmental stressors on the pathogenesis of gastrointestinal disease has received increased awareness. Stress affects different physiological functions of the gastrointestinal tract, including gastric acid secretion and mucosal blood flow. Repeated exposures of rapid-onset, highly-sustained hypergravity cause severe physical stress in the pilot. Although the effects of exposure to hypergravity on cardiovascular and cerebral functions have been the subjects of numerous studies, crucial information regarding pathophysiological changes in the gastrointestinal tract following hypergravity exposure is lacking. In this study, we investigated the effects of acute exposure to hypergravity on gastric secretory activity and gastrin release. Male Sprague-Dawley rats were exposed to +10Gz three times for 3 min. Gastric juice and blood were collected. The volume and total acidity of gastric juice, and the plasma gastrin level was measured. Acute exposure to +10Gz significantly decreased the gastric juice parameters. The gastric juice volume and total acidity of hypergravity-exposed rats were 3.54 ± 0.32 mL/100 g and 84.90 ± 5.17 mEq/L, respectively, which were significantly lower than those of the nonexposed rats (4.62 ± 0.39 mL/100 g and 97.37 ± 5.42 mEq/L; P < 0.001 and P < 0.001, respectively). In contrast, plasma gastrin level was not significantly altered following hypergravity exposure. We demonstrated that acute exposure to hypergravity led to a significant decrease in the gastric juice volume and acidity but did not alter the plasma gastrin level.

Abstract 782: A network approach to study the effect of chemical exposures on gene regulatory system in rats

Abstract Exposure to environmental chemicals during early development may increase the risk of developing breast cancer later in life. In this context, we are interested in characterizing which microRNA (miRNA) and mRNA expressions change in a coherent manner across the lifespan, and whether the co-expression pattern is affected by environmental exposures. miRNAs contribute to tumor progression via the regulation of post-transcriptional gene expressions. Thus, information on different interaction patterns among miRNAs and mRNAs measured in mammary tissues from chemical exposed vs. non-exposed rats can cast light on how chemical exposures may alter mammary gland development. Specifically, we consider three common environmental chemicals: diethyl phthalate (DEP), methyl paraben (MPB) and triclosan (TCS). Female Sprague-Dawley rats were treated with these chemicals at four windows of susceptibility (prenatal, neonatal, prepubertal and pubertal) respectively with oral doses shown to produce urinary metabolite levels similar to those measured in US population. We implemented a new algorithm, Joint Random Forest (JRF), for simultaneous estimation of multiple related networks to characterize co-expression patterns among mRNAs and miRNAs. JRF is designed to borrow information across different treatment conditions, so that regulatory relationships shared across conditions can be detected with increased power, while those specific to each condition can be detected with fewer false positives. We focused on 1403 mRNAs and 283 miRNAs with larger variability across rats, and derived four co-expression networks of these mRNAs/miRNAs for each environmental chemical treatment plus a control group. Overall we observed a substantial loss of connectivity in networks of chemical exposed groups (DEP: 1813 edges, MPB: 1539 edges and TCS: 1013 edges) compared to that of the control group (2641 edges). Interestingly, despite the overall loss of connectivity in networks of chemical exposed groups, some microRNAs such as rno-miR-126b (MIMAT0017843) and rno-miR-3596b (MIMAT0017871) showed many connecting edges in networks of chemical exposed groups but zero in that of the control group. In particular, rno-miR-3596b is a member of the Let-7 family which is well known to regulate self-renewal and tumorigenicity in breast cancer cells. Findings like this can lead to better understanding of how chemical exposures could alter gene regulatory activities. Our study also demonstrates the great potential of using JRF to investigate changes in gene regulatory system across different conditions. Citation Format: Francesca Petralia, Vasily Aushev, Kalpana Gopalakrishnan, Susan Teitelbaum, Jia Chen, Pei Wang. A network approach to study the effect of chemical exposures on gene regulatory system in rats. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 782.

Long-lasting deficits in hedonic and nucleus accumbens reactivity to sweet rewards by sugar overconsumption during adolescence.

Adolescence is a critical period characterized by major neurobiological changes. Chronic stimulation of the reward system might constitute an important factor in vulnerability to pathological development. In spite of the dramatic increase in the consumption of sweet palatable foods during adolescence in our modern societies, the long-term consequences of such exposure on brain reward processing remain poorly understood. Here, we investigated in rats the long-lasting effects of sugar overconsumption during their adolescence on their adult reactivity to the hedonic properties of sweet rewards. Adolescent rats with continuous access to 5% sucrose solution (from postnatal day 30-46) showed escalating intake. At adulthood (post-natal day 70), using two-bottle free choice tests, sucrose-exposed rats showed lower intake than non-exposed rats suggesting decreased sensitivity to the rewarding properties of sucrose. In Experiment 1, we tested their hedonic-related orofacial reactions to intraoral infusion of tasty solutions. We showed that sucrose-exposed rats presented less hedonic reactions in response to sweet tastes leaving the reactivity to water or quinine unaltered. Hence, in Experiment 2, we observed that this hedonic deficit is associated with lower c-Fos expression levels in the nucleus accumbens, a brain region known to play a central role in hedonic processing. These findings demonstrate that a history of high sucrose intake during the critical period of adolescence induces long-lasting deficits in hedonic treatment that may contribute to reward-related disorders.

Chronic Cadmium Exposure Lead to Inhibition of Serum and Hepatic Alkaline Phosphatase Activity in Wistar Rats

Alkaline phosphatase (ALP) activity in the serum and liver from rats administered with cadmium (Cd) in drinking water was studied. After metal administration, Cd showed a time-dependent accumulation in the liver, meanwhile metallothionein had a maximum increase at 1 month, remaining in this level until the end of the study. On the other hand, serum and liver ALP activity was decreased after 3 months exposure. To determine if Cd produced an inhibition on enzyme, apo-ALP prepared from both nonexposed and exposed rats was reactivated with Zn, showing 60% more activity as compared with the enzyme isolated from nonexposed rats. In vitro assays showed that Cd-ALP was partially reactivated with Zn; however, in the presence of cadmium, Zn-ALP was completely inhibited. Kinetic studies indicate a noncompetitive inhibition by Cd; these results suggest that Cd can substitute Zn, and/or Cd can interact with nucleophilic ligands essential for the enzymatic activity.

Repeated Moderate Noise Exposure in the Rat--an Early Adulthood Noise Exposure Model.

In this study, we investigated the effects of varying intensity levels of repeated moderate noise exposures on hearing. The aim was to define an appropriate intensity level that could be repeated several times without giving rise to a permanent hearing loss, and thus establish a model for early adulthood moderate noise exposure in rats. Female Sprague-Dawley rats were exposed to broadband noise for 90 min, with a 50 % duty cycle at levels of 101, 104, 107, or 110 dB sound pressure level (SPL), and compared to a control group of non-exposed animals. Exposure was repeated every 6 weeks for a maximum of six repetitions or until a permanent hearing loss was observed. Hearing was assessed by the auditory brainstem response (ABR). Rats exposed to the higher intensities of 107 and 110 dB SPL showed permanent threshold shifts following the first exposure, while rats exposed to 101 and 104 dB SPL could be exposed at least six times without a sustained change in hearing thresholds. ABR amplitudes decreased over time for all groups, including the non-exposed control group, while the latencies were unaffected. A possible change in noise susceptibility following the repeated moderate noise exposures was tested by subjecting the animals to high-intensity noise exposure of 110 dB for 4 h. Rats previously exposed repeatedly to 104 dB SPL were slightly more resistant to high-intensity noise exposure than non-exposed rats or rats exposed to 101 dB SPL. Repeated moderate exposure to 104 dB SPL broadband noise is a viable model for early adulthood noise exposure in rats and may be useful for the study of noise exposure on age-related hearing loss.

Enriched environment attenuates nicotine self-administration and induces changes in ΔFosB expression in the rat prefrontal cortex and nucleus accumbens

Environment enrichment conditions have important consequences on subsequent vulnerability to drugs of abuse. The present work examined whether exposure to an enriched environment (EE) decreases oral self-consumption of nicotine. Wistar rats were housed either in a standard environment (SE, four rats per standard cage) or in an EE during 60 days after weaning. EE consisted of eight animals housed in larger cages containing a variety of objects such as boxes, toys, and burrowing material that were changed three times a week. After this period, animals were exposed to nicotine for 3 weeks, where animals chose freely between water and a nicotine solution (0.006% in water). Fluid consumption was evaluated on a daily basis. ΔFosB immunohistochemistry in the prefrontal cortex and nucleus accumbens was also performed. Rats of the EE group consumed less nicotine solution (0.25±0.04 mg/kg/day) than SE rats (0.54±0.05 mg/kg/day). EE increased the number of ΔFos-immunoreactive (ΔFos-ir) cells in the nucleus accumbens core and shell and in the prefrontal cortex, compared with animals in the standard condition. However, rats exposed to nicotine in the SE showed higher ΔFos-ir cells in the nucleus accumbens core and shell than nonexposed rats. Nicotine consumption did not modify ΔFos-ir cells in these brain areas in EE animals. These results support the idea of a possible protective effect of the EE on reward sensitivity and the development of an addictive behavior to nicotine.

Long-term cigarette smoke exposure and the memory ability of rats of different ages

Context: Cigarette smoke had been implicated in the aetiopathogenesis of certain features seen in children. Aims: The study is aimed at assessing the effects of high doses and long-term exposure to cigarette smoke (CSE) on the memory. Settings and Design: The study involved exposed and non-exposed rats. Materials and Methods: The rats were assigned into groups A, B, C and D respectively. Each group had 5 rats. Groups A was exposed to smoke in utero only and group C from 2 to 5 months of age. Groups B and D served as the controls, respectively. Exposures to cigarette smoke was monitored at 200 PPM of carbon monoxide. Assessment of memory was done by comparing two reference time records separated by 10 minutes, obtained from the water maze task for each rat just after the entire period of exposure to cigarette smoke. Statistical Analysis Used: A paired t-test was used to assess the differences using statistical package for the social sciences software (SPSS version 15). Results: The actual reference time records revealed a statistically significant difference between the initial and final water maze task time records. All the exposed 5-month-old rats showed the lowest repeat time records and also more predictability in their repeat time records. Conclusions: Regardless of the age at the onset and duration of exposure to cigarette smoke, all the rats were able to attain memory for the first session of water task. The 5 months of exposed rat attained more memory. Hence, long-term CSE was beneficial to memory attainment.

Chronic noise stress-induced alterations of glutamate and gamma-aminobutyric acid and their metabolism in the rat brain.

Chronic stress induces neurochemical changes that include neurotransmitter imbalance in the brain. Noise is an environmental factor inducing stress. Chronic noise stress affects monoamine neurotransmitter systems in the central nervous system. The effect on other excitatory and inhibitory neurotransmitter systems is not known. The aim was to study the role of chronic noise stress on the glutamatergic and gamma-aminobutyric acid (GABA)ergic systems of the brain. Female Wistar rats (155 ± 5 g) were unintentionally exposed to noise due to construction (75-95 db, 3-4 hours/day, 5 days a week for 7-8 weeks) in the vicinity of the animal care facility. Glutamate/GABA levels and their metabolic enzymes were evaluated in different rat brain regions (cortex, hippocampus, striatum, and cerebellum) and compared with age and gender matched nonexposed rats. Chronic noise stress decreased glutamate levels and glutaminase activity 27% and 33% in the cortex, 15% and 24% in the cerebellum. Glutamate levels increased 10% in the hippocampus, 28% in striatum and glutaminase activity 15% in striatum. Glutamine synthetase activity increased significantly in all brain regions studied, that is, cortex, hippocampus, striatum, and cerebellum (P < 0.05). Noise stress-increased GABA levels and glutamate alpha decarboxylase activity 20% and 45% in the cortex, 13% and 28% in the hippocampus respectively. GABA levels and glutamate alpha decarboxylase activity decreased 15% and 14%, respectively in the striatum. GABA transaminase activity was significantly reduced in the cortex (55%), hippocampus (17%), and cerebellum (33%). Chronic noise stress differentially affected glutamatergic and GABAergic neurotransmitter systems in the rat brain, which may alter glutamate and GABA neurotransmission.

Grape juice concentrate protects reproductive parameters of male rats against cadmium-induced damage: a chronic assay

The aim of the present study was to investigate the effects of long-term grape juice concentrate (GJC) consumption, in two dosages, on the reproductive parameters of cadmium-exposed male rats. The effects of the concentrate on body mass gain, plasma testosterone levels, reproductive organ weights, daily sperm production, sperm morphology, testis histopathological and histomorphometrical parameters, and testicular antioxidant markers were investigated. Wistar rats (n 54) were distributed into six groups: CdCl2; cadmium and grape juice I (1·18g/kg per d); cadmium and grape juice II (2·36g/kg per d); grape juice I (1·18g/kg per d); grape juice II (2·36g/kg per d); control. A single dose of CdCl2 (1·2mg/kg body weight (BW)) was injected intraperitoneally and the grape juice was administered orally for 56d. The results indicated that cadmium changed all reproductive and antioxidant parameters. At dosage I (1·18g/kg BW), GJC consumption did not show the effects against cadmium-induced damages. In contrast, at dosage II (2·36g/kg BW), the GJC improved the gonadosomatic index (P=0·003), serum testosterone levels (P=0·001), the relative weight of epididymis (P=0·013) and ventral prostate (P=0·052), the percentage of normal sperm (P=0·001), and histopathological and histomorphometrical parameters. In addition, at this dosage, normalisation of the enzymatic activity of superoxide dismutase (P=0·001) and of testicular levels of glutathione (P=0·03) were observed. The parameters of the non-exposed rats did not depict significant alterations. In conclusion, the product was able to act as a protector of reproductive function against cadmium-induced damage. Such a property was expressed in a dose-dependent manner as the more effective dose was dosage II. The GJC acted possibly by antioxidant mechanisms.

Journal Digest

Journal Digest

Construction Noise Induces Hypercoagulability and Elevated Plasma Corticosteroids in Rats

Although animals housed for research purposes are strictly monitored for lighting, temperature, and humidity, the acoustic environment receives less attention. In a retrospective study, we investigated the effect of construction-induced noise on coagulation using thromboelastography in a group of healthy control rats. Animals were unintentionally exposed to noise due to construction in the vicinity of the animal care facility where these rats were housed. We compared the results to those of age-, gender-matched nonexposed rats. There was a significant shortening of the reaction (R) time (P = .009) and a trend toward an increase in coagulation index (CI; P = .09), indicating hypercoagulability. The short R time and increase in CI were correlated with an elevated plasma cortisol and corticosterone, indicating that the hypercoagulability seen in these rats is stress induced. Noise is a stress factor for which animals need to be monitored, particularly if those animals are selected as controls for hemostasis studies.

Inflammation and oxidative stress induced by cigarette smoke in Lewis rat brains

Exposure to cigarette smoke has been associated with an increased risk of neurological diseases such as stroke, Alzheimer's disease and multiple sclerosis. In these studies, serum and brain sections from Lewis rats or those exposed to cigarette smoke and control rats were examined for evidence of increased inflammation and oxidative stress. Immunocytochemical staining of brain sections from CS-exposed rats showed increased expression of class II MHC and, in ELISA, levels of IFN-gamma and TNF-α were higher than for non-exposed rats. In polymerase chain reaction assays there was increased interferon-gamma, TNF-α, IL-1α, IL-1β, IL-23, IL-6, IL-23, IL-17, IL-10, TGF-β, T-bet and FoxP3 gene expression with CS exposure. There was also markedly elevated MIP-1α/CCL3, less prominent MCP-1/CCL2 and no elevation of SDF-1α gene expression. Analysis of samples from CS-exposed and control rats for anti-oxidant expression showed no significant difference in serum levels of glutathione and, in brain, similar levels of superoxide dismutase and decreased thioredoxin gene expression. In contrast, there was increased brain gene expression for the pro-oxidants iNOS and the NADPH components NOX4, dual oxidase 1 and p22phox. Nrf2 expression, which is typically triggered as a secondary response to oxidative stress, was also increased in brains from CS-exposed rats with nuclear translocation of this protein from cytoplasm demonstrated in astrocytes in association with increased expression of the aryl hydrocarbon receptor gene, an Nrf2 target. These studies, therefore, demonstrate that CS exposure in these animals can trigger multiple immune and oxidative responses that may have important roles in the pathogenesis of CNS inflammatory neurological diseases.

Juvenile exposure to methamphetamine attenuates behavioral and neurochemical responses to methamphetamine in adult rats

Previous research has shown that children living in clandestine methamphetamine (MA) labs are passively exposed to the drug [1]. The long-term effects of this early exposure on the dopaminergic systems are unknown, but may be important for adult behaviors mediated by dopamine, such as drug addiction. The current study sought to determine if juvenile exposure to low doses of MA would lead to altered responsiveness to the stimulant in adulthood. Young male and female rats (PD20–34) were injected daily with 0 or 2mg/kg MA or left undisturbed and then tested at PD90. In the open field, adult rats exposed to MA during preadolescence had reduced locomotor activity compared to control non-exposed rats following an acute injection of MA (2mg/kg). Likewise, methamphetamine-induced dopamine increases in the dorsal striatum were attenuated in male and female rats that had been exposed to MA as juveniles, although there were no changes in basal in vivo or ex vivo dopamine levels. These findings suggest that exposure of juveniles to MA leads to persistent changes in the behavioral and neurochemical responses to stimulants in adulthood.

Spatial Frequency-Based Analysis of Mean Red Blood Cell Speed in Single Microvessels: Investigation of Microvascular Perfusion in Rat Cerebral Cortex

BackgroundOur previous study has shown that prenatal exposure to X-ray irradiation causes cerebral hypo-perfusion during the postnatal development of central nervous system (CNS). However, the source of the hypo-perfusion and its impact on the CNS development remains unclear. The present study developed an automatic analysis method to determine the mean red blood cell (RBC) speed through single microvessels imaged with two-photon microscopy in the cerebral cortex of rats prenatally exposed to X-ray irradiation (1.5 Gy).Methodology/Principal FindingsWe obtained a mean RBC speed (0.9±0.6 mm/sec) that ranged from 0.2 to 4.4 mm/sec from 121 vessels in the radiation-exposed rats, which was about 40% lower than that of normal rats that were not exposed. These results were then compared with the conventional method for monitoring microvascular perfusion using the arteriovenous transit time (AVTT) determined by tracking fluorescent markers. A significant increase in the AVTT was observed in the exposed rats (1.9±0.6 sec) as compared to the age-matched non-exposed rats (1.2±0.3 sec). The results indicate that parenchyma capillary blood velocity in the exposed rats was approximately 37% lower than in non-exposed rats.Conclusions/SignificanceThe algorithm presented is simple and robust relative to monitoring individual RBC speeds, which is superior in terms of noise tolerance and computation time. The demonstrative results show that the method developed in this study for determining the mean RBC speed in the spatial frequency domain was consistent with the conventional transit time method.

Effects of 3,3′,4,4′,5-pentachlorobiphenyl (PCB126) on vertebral bone mineralization and on thyroxin and vitamin D levels in Sprague–Dawley rats

The aim of the present study is to use Fourier transform infrared spectrometry (FTIR), and transmission electron microscopy (TEM) techniques, to make a more detailed description of toxic effects of 3,3',4,4',5-pentachlorobiphenyl (PCB126) on bone tissue at the microstructural and at the molecular level as a result of an altered bone metabolism. We have analysed potential changes on vitamin D and thyroxin serum levels since these hormones represent endocrine endpoints that are critical for bone growth and development. For this purpose Sprague-Dawley rats were exposed (n=10) to PCB126 (i.p.) for 3 months (total dose, 384microg/kg bodyweight), while control rats (n=10) were injected with corn oil (vehicle). Results from FTIR showed that vertebrae from the exposed rats had an overall lower degree of mineralization (-8.5%; p<0.05) compared with the controls. In addition, results from peripheral quantitative computed tomography (pQCT) analyses showed significant increases in the trabecular bone mineral density (+12%; p<0.05) in the exposed group compared with the controls. The TEM analyses also showed an alteration in the crystallinity properties of vertebral bone mineral with a significant decrease in the size and crystallinity of apatite crystal forming the bone tissue in the exposed vs. non-exposed rats. Serum analysis revealed lower levels of thyroid hormones, FT4 (-42%; p<0.005), TT4 (-26%; p<0.005), and vitamin D (-21%; p<0.005) in exposed group compared to control animals. The complementary techniques (TEM and FTIR) used in this study have revealed insights into possible bone mineralization alteration due to PCB126 exposure. The lowering of both the thyroxin and vitamin D serum levels might be an underlying explanation for the observed effects on bone mineralization.

Exposure to radiation from global system for mobile communications at 1,800 MHz significantly changes gene expression in rat hippocampus and cortex

We have earlier shown that radio frequency electromagnetic fields can cause significant leakage of albumin through the blood–brain barrier of exposed rats as compared to non-exposed rats, and also significant neuronal damage in rat brains several weeks after a 2 h exposure to a mobile phone, at 915 MHz with a global system for mobile communications (GSM) frequency modulation, at whole-body specific absorption rate values (SAR) of 200, 20, 2, and 0.2 mW/kg. We have now studied whether 6 h of exposure to the radiation from a GSM mobile test phone at 1,800 MHz (at a whole-body SAR-value of 13 mW/kg, corresponding to a brain SAR-value of 30 mW/kg) has an effect upon the gene expression pattern in rat brain cortex and hippocampus—areas where we have observed albumin leakage from capillaries into neurons and neuronal damage. Microarray analysis of 31,099 rat genes, including splicing variants, was performed in cortex and hippocampus of 8 Fischer 344 rats, 4 animals exposed to global system for mobile communications electromagnetic fields for 6 h in an anechoic chamber, one rat at a time, and 4 controls kept as long in the same anechoic chamber without exposure, also in this case one rat at a time. Gene ontology analysis (using the gene ontology categories biological processes, molecular functions, and cell components) of the differentially expressed genes of the exposed animals versus the control group revealed the following highly significant altered gene categories in both cortex and hippocampus: extracellular region, signal transducer activity, intrinsic to membrane, and integral to membrane. The fact that most of these categories are connected with membrane functions may have a relation to our earlier observation of albumin transport through brain capillaries.

Lipid metabolism in liver of rat exposed to cadmium

We investigated the effect of exposition to cadmium (Cd, 15ppm for 8 weeks) through drinking water on liver lipid metabolism in adult male Wistar rats. As compared to metal non-exposed (control) rats, the serum triglycerides, cholesterol and LDL+VLDL cholesterol concentrations increased. This was associated to a decrease of lipoprotein lipase activity in post heparinic plasma. The VLDL secretion from liver was not modified. Cd treatment increased triglycerides and decreased esterified cholesterol contents in liver. The high triglyceride mass was related to the increased glycerol-3-phosphate acyltransferase mRNA expression. In addition, the liver fatty acids synthesis increased, as determined by an increment of fatty acid synthetase and isocitrate dehydrogenase activities, and [14C]-acetate incorporation into saponifiable lipid fraction. The relative percentage of palmitic acid (16:0) and total saturated fatty acids were increased compared with control. Hepatic glucose-6-phosphate dehydrogenase, malic dehydrogenase and cholesteryl ester hydrolase activities were unchanged.In liver, the Cd treatment decreased triglyceride and cholesterol in mitochondria, also increased triglyceride in cytosol, and cholesterol and phospholipid contents in nuclei, compared with control. In addition, an increase of nuclei phosphatidylcholine synthesis was observed. Cd exposure alters directly or indirectly the serum lipid content and liver lipid metabolism.