Young Male Albino Rats Research Articles

Elimination of high-refined-sugar diet as treatment strategy for autistic features induced in a rodent model

Purpose: To investigate the potency of ampicillin in altering gut flora in the presence of a high-sucrose diet in rat pups, and to determine its effect on selected neurotransmitters and a cytokine as markers of the persistent autistic features repeatedly induced in orally administered propionic acid rat pups..Methods: Twenty-eight young male Wistar albino rats were divided into four equal groups. The first group served as a control. The second group received an oral neurotoxic dose of propionic acid (PPA, 250 mg/kg body weight/day) for 3 days. The third group was treated with ampicillin (50 mg/kg for 3 weeks) with a standard diet. The fourth group was given the same dose of ampicillin with a high-sucrose diet for 10 weeks.Results: The results showed a significant (p < 0.001) decrease in the investigated neurotransmitters in PPA- and ampicillin-treated rat pups (norepinephrine by 32.49 and 14.58 %, dopamine by 31.45 and 20.22 %, serotonin by 35.99 and 29.09 %), as well as a remarkable increase (p < 0.001) in the proinflammatory cytokine, IL-6 (30.07and 6.07 %). The high-sucrose diet also significantly (p < 0.001) enhanced the neurotoxic effect of ampicillin.Conclusion: The observed dietary modulation of the gut microbiota, coupled with the subsequent modulation of brain neurochemistry and inflammation, demonstrates the considerable potential of dietary intervention through the elimination of highly refined sugar as a treatment strategy to prevent and treat autism.Keywords: Neurotoxicity, Ampicillin, Propionic acid, Neurotransmitters, Cytokines, High-sucrose diet

Effect of orally administered zinc oxide nanoparticles on albino rat thymus and spleen.

This study aimed to evaluate the toxicological effects of oral intake of Zinc oxide nanoparticles (ZnO NPs) on the structure of thymus and spleen. Twenty-four young male Wistar albino rats were assigned into two groups: group I (control) and group II (ZnO NPs treated group).The thymus and spleen were analyzed biochemically, histopathologically and immunohistochemically. After ZnO NPs intake, hematologically, the total leucocytic count was significantly increased while the RBCs and platelets counts and Hb % were significantly decreased. Biochemically, a significant decrease in serum total antioxidant capacity and anti-inflammatory cytokines including interleukin 4 and 10 (IL-4 and IL-10) levels was noted. While a significant increase in splenic and thymic malondialdehyde (MDA) and DNA shearing, as well as the studied proinflammatory cytokines; IL-1β, tumor necrotic factor (TNF-α) and interferon (INF-γ) levels was detected. Notably, we noted upregulation of the immunomodulatory [CD3, CD11b, heme oxygenase (HO-1)] and the inflammatory [toll-like receptor 4 and 6 (TLR4 and TLR6)] genes. Histopathologically, degenerative changes were detected in thymus and spleen of ZnO NPs treated group. While the immunohistochemical analysis of the ZnO NPs treated group revealed a decrease in the number of cells expressed positive reactions of anti-PCNA and an increase in the number of cells expressed positive reaction of anti-p53 in the thymus and spleen. In conclusion, ZnO NPs induced obvious immunotoxicity in the thymus and spleen, where oxidative/inflammatory pathway may be the potential mechanism underlying this immunotoxicity. © 2017 IUBMB Life, 69(7):528-539, 2017.

Glutamate excitotoxicity induced by orally administered propionic acid, a short chain fatty acid can be ameliorated by bee pollen

BackgroundRodent models may guide investigations towards identifying either environmental neuro-toxicants or drugs with neuro-therapeutic effects. This work aims to study the therapeutic effects of bee pollen on brain glutamate excitotoxicity and the impaired glutamine-glutamate- gamma amino butyric acid (GABA) circuit induced by propionic acid (PPA), a short chain fatty acid, in rat pups.MethodsTwenty-four young male Western Albino rats 3–4 weeks of age, and 45–60 g body weight were enrolled in the present study. They were grouped into four equal groups: Group 1, the control received phosphate buffered saline at the same time of PPA adminstration; Group 2, received 750 mg/kg body weight divided into 3 equal daily doses and served as acute neurotoxic dose of PPA; Group 3, received 750 mg/kg body weight divided in 10 equal doses of 75 mg/kg body weight/day, and served as the sub-acute group; and Group 4, the therapeutic group, was treated with bee pollen (50 mg/kg body weight) for 30 days after acute PPA intoxication. GABA, glutamate and glutamine were measured in the brain homogenates of the four groups.ResultsThe results showed that PPA caused multiple signs of excitotoxicity, as measured by the elevation of glutamate and the glutamate/glutamine ratio and the decrease of GABA, glutamine and the GABA/glutamate ratio. Bee pollen was effective in counteracting the neurotoxic effects of PPA to a certain extent.ConclusionIn conclusion, bee pollen demonstrates ameliorating effects on glutamate excitotoxicity and the impaired glutamine-glutamate-GABA circuit as two etiological mechanisms in PPA-induced neurotoxicity.

Adverse Effects of Two Kinds of Food Additive Mixtures (Flavor Enhancer, Food Preservative or Food Coloring Agent) on Physiological Parameters in Young Male Albino Rats

Background: food additives are substances used in food industry in order to improve the food’s taste, appearance by preserving its flavor and preventing it from souring. Food additives are added to the most junk and fast foods, especially food for kids. Aim of the work: this work was aimed to investigate the adverse effects of some food additives on the biochemical parameters in addition to study the side effects of these food additives in male albino rats. Materials and Methods: this study was performed on twenty four young male albino rats with an average 120-145 g body weight. Animals were divided into four groups (6 /cage); Group I (Control untreated group), Group II (administered orally with sodium nitrite (0.1 mg/kg b.wt./day) and annatto (0.065 mg/kg b.wt./day)), Group III (administered orally with sodium nitrite (0.1 mg/kg b.wt./day) and monosodium glutamate (MSG) (15 mg/kg b.wt./day)) and Group IV (administered orally with annatto (0.065 mg/kg b.wt./day) and monosodium glutamate (15 mg/kg b.wt./day)). Blood samples were collected on the last day of experiment, for biochemical estimations which included levels of serum glucose, total protein (TP), albumin, creatinine, urea, testosterone , thyroid hormones (T3 and T4), activities of AST and ALT in addition to lipid profile. Results: showed marked elevation in levels of fasting glucose, activities of AST, ALT, urea, creatinine, total cholesterol (TC), triglycerides (TG) and high density lipoprotein cholesterol (HDL-C), VLDL and ratios of TC/HDL-C and LDL-C/HDL-C (risk factors) as well as albumin / globulin ratio and serum thyroid hormones (T3 & T4) accompanied with marked decline in levels of serum total proteins, albumin, globulin, albumin/ creatinine ratio, testosterone and HDL-C in all treated groups in comparison to the control group. There was a significant reduction in the body weight in groups that received (NaNO2 with annatto) and (MSG with NaNO2) while treated rats with (MSG and annatto) showed a significant increase in body weight as compared to control rats. Conclusion:Due to the harmful effects of food additives, the use of these compounds must be limited as it resulted in a vehement disturbance in the biochemical and physiological parameters that was grievously pronounced on many hormones.

Effects of Some Food Additives on Some Biochemical Parameters in Young Male Albino Rats and the Ameliorative Role of Royal Jelly

Background: the use of food additives is one of the most important problems in the human health nutrition field. Food additives are widely used for various purposes; including preservation, coloring, and sweetening, however, the physiological and biochemical changes may be produced. Aim of the work: was to investigate the protective role of royal jelly (RJ) against abnormalities in metabolic biochemical parameters that induced by these food additives in male albino rats. Materials and Methods: thirty young male albino rats with an average body weight 120-140 g were divided into three groups (10/cage); Group I: served as normal control group, Group II: rats orally administrated with the mixture which consists of sodium nitrite (NaNO2 0.1 mg/kg b.wt./ day), annatto (0.065 mg/kg b.wt./day) and monosodium glutamate (MSG 15 mg/kg b.wt./day) and Group III: rats orally administrated with the previous mixture and then orally administrated with royal jelly (14.28 mg/kg b.wt./day soluble in maize oil). At the end of the experiment, blood samples were collected for biochemical estimations which including levels of serum glucose, creatinine, urea, testosterone, thyroid hormones (T3 and T4), activities of AST and ALT, total protein (TP), albumin, total cholesterol, triglycerides, high-density lipoprotein (HDL-c) and low-density lipoprotein (LDL-c). Results: the present study showed marked elevation in levels of fasting blood glucose, activities of AST, ALT, levels of serum urea, creatinine, TC, TG, LDL-c, VLDLand ratios of TC/HDL-c and LDL-c/HDL-c (risk factors) as well as albumin /globulin ratio and serum thyroid hormones (T3&T4) accompanied with significant reduction in the body weight, serum total proteins, albumin, globulin, albumin/creatinine, testosterone and HDL-C concentrations in the group that administrated with the mixture which consists of (NaNO2, MSG and annatto) as compared to control rats. While administration with royal jelly significantly ameliorated the disturbed biochemical parameters and showed significant improvement in most of these parameters. Conclusion: it could be concluded that royal jelly offers a therapeutic advantage that minimizes the metabolic abnormalities and biochemical changes which induced by these food additives.

The ability of hesperidin compared to that of insulin for preventing osteoporosis induced by type I diabetes in young male albino rats: A histological and biochemical study

BackgroundPatients with type I diabetes are at increased risk of osteoporosis even after insulin therapy in adult stage. This study was conducted to compare the efficacy of hesperidin (hesp) therapy versus that of insulin alone in the alleviation of osteoporosis arising from type I diabetes mellitus (T1DM) in young rats. Materials and methodsHesperidin was administered orally to STZ-induced diabetes. The animals were evaluated morphologically and biochemically and compared with that received daily SC injections of long-acting insulin. ResultsHistologically, we observed the degeneration of osteoblasts and osteocytes, decreased collagen fibers, and disturbed bone turn over markers in untreated DM rats. Hesperidin+ insulin supplementation to diabetic rats caused significant improvement of most of the bone histological and morphometric parameters compared with the insulin-treated group. Furthermore, hesp treatment significantly reduced pro-inflammatory mediators TNFα and NF-κB and increased serum biochemical markers of bone turnover, including osteopontin (OPN), osteocalcin (OC) and decreased serum alkaline phosphatase (ALP). ConclusionThese data demonstrated that hesp could be considered to be a beneficial drug for preventing diabetic osteoporosis in growing age.

Effect of monosodium glutamate on body weight and the histological structure of the zona fasciculata of the adrenal cortex in young male albino rats

Introduction Monosodium glutamate (MSG) is commonly used as a flavor enhancer in both home and restaurant cooking. Aim The aim of this work was to clarify the possible effect of MSG administration on the body weight and the histological structure of the zona fasciculata (ZF) of the adrenal cortex in young male albino rats and to assess whether or not this effect was reversible. Materials and methods A total of 40 male albino rats aged 4 weeks were weighed at the onset of the study and then divided into two equal groups. The control rats (group I) were held without medication either for 2 weeks (group Ia) or for 4 weeks (group Ib) and then killed. The experimental rats (group II) received a daily oral dose of MSG (4 mg/g body weight) dissolved in 3 ml of distilled water for 2 weeks and then 10 of them were killed 2 h after the last dose (group IIa); the other 10 rats were held without medication for another 2 weeks and then killed (group IIb). All rats were weighed before scarification. Sections of the adrenal glands were examined with light and electron microscopes. Thickness of the ZF was measured in all subgroups. Data of the final body weight and ZF thickness were analyzed as mean±SD and P values were calculated. Results Statistically, the final body weight of rats increased in both groups IIa and IIb and also the thickness of the ZF increased in group IIa as compared with their controls. Histologically, group IIa showed loss of the cord-like architecture of ZF cells. They appeared distended with highly vacuolated cytoplasm that was ultrastructurally full of lipid droplets. Group IIb revealed partial improvement and retained normal thickness and structure of the ZF. Conclusion MSG causes histopathological changes in the ZF of the adrenal cortex, increasing its thickness and its secretion, and this could explain the increased final body weight. These changes are reversible but may need a long time to regain their normal values.

English

Cimetidine is a potent histaminic H2-receptor antagonist extensively prescribed for ulcers. It has also known as reproductive toxicant as indicated by significantly reduced weight of accessory sex organs and is responsible for sexual dysfunction. The present study was designed to investigate the influence of parenterally administered drugs cimetidine and bromocriptine on the germinal epithelium of adult male albino rats and its relation with spermatogenesis. Ninety adult young male albino rats between the ages of 60 to 120 days were selected for the study and divided into three groups as Group A, B & C. The spermatogenesis was normal in almost all of the tubules of group B but a few of them were seen lined with only Sertoli cells and all the other germ cells like spermatogonia, primary spermatocyes, spermatids early and late, and spermatozoa were absent indicating total atrophy with both Sertoli cells and Leydig cells hyperplasia. However, the seminiferous tubules of group C were showing disorganisation/ disruption or both at the level of basal compartment of germinal epithelium in small quadrants, a quarter, half or more than half of their tubules indicating partial atrophy. Both normal and abnormal germinal epithelium was seen in same/different tubules but a few of them were seen lined with only Sertoli cells and all the other germ cells like spermatogonia, primary spermatocytes, spermatids early and late, and spermatozoa were absent. From our findings, we could not exclude the possibility that besides the known anti-androgenic effect of cimetidine, a possible interference of cimetidine on the histoarchitecture of the seminiferous epithelium, as well as lack of other biochemical factors essential for spermatogenesis could be involved in the testicular changes/ alterations of both groups B and C.

Potency of pre–post treatment of coenzyme Q10 and melatonin supplement in ameliorating the impaired fatty acid profile in rodent model of autism

BackgroundAbnormalities in fatty acid metabolism and membrane fatty acid composition play a part in a wide range of neurodevelopmental and psychiatric disorders. Altered fatty acid homeostasis as a result of insufficient dietary supplementation, genetic defects, the function of enzymes involved in their metabolism, or mitochondrial dysfunction contributes to the development of autism.ObjectiveThis study evaluates the association of altered brain lipid composition and neurotoxicity related to autism spectrum disorders in propionic acid (PA)–treated rats.DesignForty-eight young male western albino rats were used in this study. They were grouped into six equal groups with eight rats in each. The first group received only phosphate buffered saline (control group). The second group received a neurotoxic dose of buffered PA (250 mg/kg body weight/day for 3 consecutive days). The third and fourth groups were intoxicated with PA as described above followed by treatment with either coenzyme Q (4.5 mg/kg body weight) or melatonin (10 mg/kg body weight) for 1 week (therapeutically treated groups). The fifth and sixth groups were administered both compounds for 1 week prior to PA (protected groups). Methyl esters of fatty acid were extracted with hexane, and the fatty acid composition of the extract was analyzed on a gas chromatography.ResultsThe obtained data proved that fatty acids are altered in brain tissue of PA-treated rats. All saturated fatty acids were increased while all unsaturated fatty acids were significantly decreased in the PA-treated group and relatively ameliorated in the pre–post melatonin and coenzyme Q groups.ConclusionsMelatonin and coenzyme Q were effective in restoring normal level of most of the impaired fatty acids in PA-intoxicated rats which could help suggest both as supplements to ameliorate the autistic features induced in rat pups.

Biochemical and Spectral Analysis of Roridin A Toxin and Copper (I) Nicotinate Complex as Antidote on Male Rat Liver

This work has been designed to evaluate the curative effect of copper (I) –nicotinate complex on the hepatotoxicity of Roridin A in male rats as well as the study of the spectral analysis of this complex. Healthy young male albino rats (n=40) were exposed to a single dose of Roridin A (60 μg/kg body weight) and scarified and another group was treated with the copper (I) –nicotinate complex. Such intoxication resulted in some biochemical parameters such as ALP, GGT, TAS, Ferritin and AFP. Finally, Copper (I)-Nicotinate complex reduced many undesired changes of liver tissue and this improvement was predicted since this complex has been confirmed previously as a therapeutic agent against induced mycotoxins as Roridin A.

Effects of GSM modulated radio-frequency electromagnetic radiation on permeability of blood–brain barrier in male & female rats

With the increased use of mobile phones, their biological and health effects have become more important. Usage of mobile phones near the head increases the possibility of effects on brain tissue. This study was designed to investigate the possible effects of pulse modulated 900MHz and 1800MHz radio-frequency radiation on the permeability of blood–brain barrier of rats. Study was performed with 6 groups of young adult male and female wistar albino rats. The permeability of blood-brain barrier to intravenously injected evans blue dye was quantitatively examined for both control and radio-frequency radiarion exposed groups. For male groups; Evans blue content in the whole brain was found to be 0.08±0.01mg% in the control, 0.13±0.03mg% in 900MHz exposed and 0.26±0.05mg% in 1800MHz exposed animals. In both male radio-frequency radiation exposed groups, the permeability of blood–brain barrier found to be increased with respect to the controls (p<0.01). 1800MHz pulse modulated radio-frequency radiation exposure was found more effective on the male animals (p<0.01). For female groups; dye contents in the whole brains were 0.14±0.01mg% in the control, 0.24±0.03mg% in 900MHz exposed and 0.14±0.02mg% in 1800MHz exposed animals. No statistical variance found between the control and 1800MHz exposed animals (p>0.01). However 900MHz pulse modulated radio-frequency exposure was found effective on the permeability of blood-brain barrier of female animals. Results have shown that 20min pulse modulated radio-frequency radiation exposure of 900MHz and 1800MHz induces an effect and increases the permeability of blood-brain barrier of male rats. For females, 900MHz was found effective and it could be concluded that this result may due to the physiological differences between female and male animals. The results of this study suggest that mobile phone radation could lead to increase the permeability of blood-brain barrier under non-thermal exposure levels. More studies are needed to demonstrate the mechanisms of that breakdown.

Study the effects of radon inhalation on biomechanical properties of blood in rats

Purpose: To investigate the effect of inhalation radon gas (Rn) on the biomechanical properties of red blood cell of rats. Methods: 20 young healthy adult male albino rats were divided into equally 4 groups. The first group (0) served as control group, while the other three groups (I, II and III) were exposed to Rn gas inside a chamber for 3, 5 and 7 weeks. The biomechanical properties of red blood cell of rats was performed by determine the rheological properties of blood and the osmotic fragility of red blood cells (RBCs). Results: The Rn doses received by every group of rats were found to 34.84, 58.07 and 81.30 mSv for 3, 5 and 7 weeks respectively (based on 12 exposure hours per week). The obtained results indicate that the viscosity, consistency index, yield stress and aggregation index increase with Rn doses. The osmotic fragility curves of irradiated groups shift toward lower values of NaCl concentration. The dispersion of hemolysis (S) increased, at the same time an average osmotic fragility (H 50% ) decreased. Conclusion: The results indicates that the exposure to radon alters the mechanical properties of red blood cells membrane (permeability and elasticity) reflecting a change in its physiological properties. This mean that low levels of Rn gas are harmful to biological systems and the degree of damage was dose-dependent.

The neurotoxic effects of ampicillin-associated gut bacterial imbalances compared to those of orally administered propionic acid in the etiology of persistent autistic features in rat pups: effects of various dietary regimens.

HypothesisA healthy gut with normal intestinal microflora is completely disrupted by oral antibiotics. The byproducts of harmful gut bacteria can interfere with brain development and may contribute to autism. Strategies to improve the gut microflora profile through dietary modification may help to alleviate gut disorders in autistic patients.MethodSixty young male western albino rats were divided into six equal groups. The first group served as the control; the second group was given an oral neurotoxic dose of propionic (PPA) (250 mg/kg body weight/day) for three days. The third group received an orogastric dose of ampicillin (50 mg/kg for three weeks) with a standard diet. Groups 4, 5 and 6 were given an orogastric dose of ampicillin and fed high-carbohydrate, high-protein and high-lipid diets, respectively, for 10 weeks. Biochemical parameters related to oxidative stress were investigated in brain homogenates from each group.ResultThe microbiology results revealed descriptive changes in the fecal microbiota of rats treated with ampicillin either alone or with the three dietary regimens. The results of PPA acid and ampicillin treatment showed significant increases in lipid peroxidation and catalase with decreases in glutathione and potassium compared with levels in the control group. A protein-rich diet was effective at restoring the glutathione level, while the carbohydrate-rich diet recovered lipid peroxidation and catalase activity. In addition, the three dietary regimens significantly increase the potassium level in the brain tissue of the test animals. Lactate dehydrogenase was remarkably elevated in all groups relative to the control. No outstanding effects were observed in glutathione S-transferase and creatine kinase.ConclusionThe changes observed in the measured parameters reflect the neurotoxic effects of PPA and ampicillin. Lipid peroxide and catalase activity and the levels of glutathione and potassium are satisfactory biomarkers of PPA and ampicillin neurotoxicity. Based on the effects of the three dietary regimens, a balanced diet can protect against PPA or ampicillin-induced neurotoxicity that might induce autistic traits. These outcomes will help efforts directed at controlling the prevalence of autism, a disorder that has recently been associated with PPA neurotoxicity.

Neuroprotective Effects of Purslane Seeds against Adverse Effects Induced by Experimental Hyperlipidemia on Frontal Cortex and Cerebellum in Young Male Albino Rats

Background. Hyperlipidemia is characterized by abnormally elevated levels of lipids and is positively associated with cerebrovascular diseases. Alzheimer’s disease (AD) is a chronic brain disorder characterized by cognitive impairment, inflammation, β-amyloid deposition, and vascular damage. Recent studies have shown that high cholesterol levels are linked to the pathology of AD. Purslane seeds are medicinal plants rich in unsaturated fatty acids (omega-3), antioxidants, and fibers. They are known to have antidiabetic and antiatherogenic activities. The aim of this research is to study the structural alterations occurring in the frontal cortex and cerebellum after feeding high cholesterol diet, and the possible protective role of purslane seeds. Materials and methods. Forty male albino rats were used in the study. They were divided into three groups; control group (20 rats), hypercholesterolemic group (10 rats) who were fed the balanced diet supplemented with cholesterol at a dose of 2 gm/100 gm diet, and protected group (10 rats) who were fed the same previous hypercholesterolemic diet concomitant with purslane seed 20% (20 gm/100 ml water). After 3 months, blood samples were collected from all rats for biochemical estimation and fresh specimens were taken from the frontal cortex and cerebellum of each rat and processed for; light microscopic examination using H&E and Orcein stains. Results. Significant increase of serum triglyceride (TG), total cholesterol (TC), and low-density lipoprotein (LDL-C) levels in hyperlipidemic rats were detected. Associated structural changes in the frontal cortex of the rats were evident as pyknotic nuclei of degenerated neurons, loss of neuron, dilation and congestion of blood vessels, expanded perivascular space, and increased vacuolar spaces of neuropil. The cerebellar cortex of the rats fed on high cholesterol diet revealed pyknotic nuclei of degenerated neuron and decrease in the number of Purkinje and granule cells compared to the control group. Concomitant administration of purslane seeds revealed evident amelioration of biochemical and most of the structural changes. Conclusion. We concluded that a high cholesterol diet has deleterious biochemical changes associated with structural alteration in the frontal cortex and cerebellum and purslane seeds ameliorate most of these changes.

Effect of homocysteine on the histological structure of femur in young male albino rats and the possible protective role of folic acid

Abstract Introduction: Homocysteine (HCY) is an amino acid that is formed as an intermediate during the metabolism of methionine. The role of hyperhomocysteinemia in the pathogenesis of osteoporosis has been considered

Physiological Effects of Some Artificial and Natural Food Coloring on Young Male Albino Rats

Food colorants are widely added to food in order to attract the consumer. Recent researches have incriminated these additives for causing some problems to human health. This study was conducted to determinate the physiological effects of some natural (curcumin, carrotin and curcumin) and synthetic (tetrazine, sunset yellow and erythosine) food colorants on some hematological and biochemical parameters of male albino rats (rattus norvegicus, spraguedawlay strain). Results revealed that administration of synthetic food colorants decreased the percentage of high density lipoprotein cholesterol (HDL-C), glutathione secretion (GSH), superoxide dismutase (SoD), and plasma immune-system and significantly increased plasma lipid lipoprotein, total cholesterol (LDL-C), lipid peroxidase, blood glucose, plasma urea and creatinine and increased activities of alkaline phosphatase, acid phosphatase, and lactate dehydrogenase. Hence, it is recommended to avoid adding synthetic colorants as additive to foodstuff, while natural colorants seemed to be the best choice as food colorants.

Effect of Vitamin E Administration on Learning of the Young Male Rats

The effect of vitamin E intake on spatial learning and working memory performances of young rats has been investigated in the Morris water maze and locomotor activity has been assessed by an open-field test. A total of 45 young male Wistar albino rats aged two months were divided into three equal groups: control, olive oil, and vitamin E groups. These groups were treated for 30 days with a once daily intraperitoneal injection. The rats were then tested for their ability to find the location of the platform (spatial learning). The results revealed that there was no statistically significant difference between the time spent to find the platform and the time spent in half area of the tank, including the platform among the group, while the time spent to find the platform was found to have increased from the first day to the fourth day in all the groups. In the open-field test, the locomotor activity quite significantly increased in the peripheral area in the olive oil group. The supplementation with vitamin E for a short period had not improved the learning performance of the healthy young rats. It was concluded that the beneficial effect of vitamin E intake on learning is related to the beginning time and the duration of vitamin E intake.

Protective and restorative potency of Vitamin D on persistent biochemical autistic features induced in propionic acid-intoxicated rat pups.

BackgroundReducing exposure to toxic environmental agents is a critical area of intervention. Prenatal or postnatal exposure to certain chemicals has been documented to increase the risk of autism spectrum disorder. Propionic acid (PA) found in some foods and formed as a metabolic product of gut microbiota has been reported to mediate the effects of autism. Results from animal studies may help to identify environmental contaminants and drugs that produce or prevent neurotoxicity, and may thereby aid in the treatment of neurodevelopmental disorders such as autism. The present study investigated the protective and/or therapeutic effects of vitamin D against brain intoxication induced by propionic acid (PPA) in rats.MethodsTwenty-eight young male Western Albino rats were enrolled in the present study. They were grouped into four equal groups of 7. The control group received only phosphate buffered saline; the oral buffered PPA-treated group received a neurotoxic dose of 250 mg/kg body weight/day for 3 days; and the Vitamin D-protected group received 1000 IU/kg/day of alpha, 25-dihydroxyvitamin D (3) (1, 25-VD) for two weeks, after which the rats were injected with PPA 250 mg/Kg body weight/day for 3 days. The fourth group received PPA 250 mg/Kg body weight/day for 3 days followed by alpha, 25-dihydroxyvitamin D (3) (1, 25-VD) for two weeks (Vitamin D therapeutic effect). Vitamin D and calcium were measured in the plasma of the four studied groups. Serotonin, interferon gamma (IFN-γ), glutathione-s-transferase activity and DNA double helix breaks were assayed in the brain tissue of the rats for all groups.ResultsThe obtained data showed that the PPA-treated group demonstrated higher plasma vitamin D levels compared to the control rats, together with multiple signs of brain toxicity, as indicated by a depletion of serotonin (5HT), an increase in IFN-γ and inhibition of glutathione-s-transferase activity as three biomarkers of brain dysfunction. Additionally, Comet DNA assays showed remarkably higher tail length, tail DNA % damage and tail moment as a neurotoxic effect of PPA.ConclusionsVitamin D showed a greater protective than therapeutic effect on PPA-induced neurotoxicity in rats, as there was a remarkable amelioration of the impaired biochemically measured parameters representing neurochemical, inflammation, and detoxification processes.

Selected biomarkers as predictive tools in testing efficacy of melatonin and coenzyme Q on propionic acid - induced neurotoxicity in rodent model of autism.

BackgroundExposures to environmental toxins are now thought to contribute to the development of autism spectrum disorder. Propionic acid (PA) found as a metabolic product of gut bacteria has been reported to mimic/mediate the neurotoxic effects of autism. Results from animal studies may guide investigations on human populations toward identifying environmental contaminants that produce or drugs that protect from neurotoxicity. Forty-eight young male Western Albino rats were used in the present study. They were grouped into six equal groups 8 rats each. The first group received a neurotoxic dose of buffered PA (250 mg/Kg body weight/day for 3 consecutive days). The second group received only phosphate buffered saline (control group). The third and fourth groups were intoxicated with PA as described above followed by treatment with either coenzyme Q (4.5 mg/kg body weight) or melatonin (10 mg/kg body weight) for one week (therapeutically treated groups). The fifth and sixth groups were administered both compounds for one week prior to PA (protected groups). Heat shock protein70 (Hsp70), Gamma amino-butyric acid (GABA), serotonin, dopamine, oxytocin and interferon γ-inducible protein 16 together with Comet DNA assay were measured in brain tissues of the six studied groups.ResultsThe obtained data showed that PA caused multiple signs of brain toxicity revealed in depletion of GABA, serotonin, and dopamine, are which important neurotransmitters that reflect brain function, interferon γ-inducible protein 16 and oxytocin. A high significant increase in tail length, tail DNA% damage and tail moment was reported indicating the genotoxic effect of PA. Administration of melatonin or coenzyme Q showed both protective and therapeutic effects on PA–treated rats demonstrated in a remarkable amelioration of most of the measured parameters.ConclusionIn conclusion, melatonin and coenzyme Q have potential protective and restorative effects against PA-induced brain injury, confirmed by improvement in biochemical markers and DNA double strand breaks.

Protective and therapeutic potency of N-acetyl-cysteine on propionic acid-induced biochemical autistic features in rats

BackgroundThe investigation of the environmental contribution for developmental neurotoxicity is very critical. Many environmental chemical exposures are now thought to contribute to the development of neurological disorders, especially in children. Results from animal studies may guide investigations of human populations towards identifying either environmental toxicants that cause or drugs that protect from neurotoxicity and may help in treatment of neurodevelopmental disorders.ObjectiveTo study both the protective and therapeutic effects of N-acetyl cysteine on brain intoxication induced by propionic acid (PPA) in rats.MethodsTwenty-eight young male Western Albino rats were enrolled in the present study. They were grouped into four equal groups, each of 7 animals. Group 1: control group, orally received only phosphate buffered saline; Group 2: PPA-treated group, received a neurotoxic dose of of PPA of 250 mg/kg body weight/day for 3 days; Group 3: protective group, received a dose of 50 mg/kg body weight/day N-acetyl-cysteine for one week followed by a similar dose of PPA for 3 days; and Group 4: therapeutic group, treated with the same dose of N-acetyl cysteine after being treated with the toxic dose of PPA. Serotonin, interferon gamma (IFN-γ), and glutathione-s-transferase activity, together with Comet DNA were assayed in the brain tissue of rats in all different groups.ResultsThe obtained data showed that PPA caused multiple signs of brain toxicity as measured by depletion of serotonin (5HT), increase in IFN-γ and inhibition of glutathione-s-transferase activity as three biomarkers of brain dysfunction. Additionally Comet DNA assay showed remarkably higher tail length, tail DNA % damage and tail moment. N-acetyl-cysteine was effective in counteracting the neurotoxic effects of PPA.ConclusionsThe low dose and the short duration of N-acetyl-cysteine treatment tested in the present study showed much more protective rather than therapeutic effects on PPA-induced neurotoxicity in rats, as there was a remarkable amelioration in the impaired biochemical parameters representing neurochemical, inflammatory, detoxification and DNA damage processes.