Rats Received Corn Oil Research Articles

The Possible Protective Effect of Taurine on Bisphenol Induced Structural Changes on the Cerebral Cortex of Rats: Histological and Immunohistochemical Study.

Bisphenol A (BPA) is a chemical compound that has been used in many industries, such as paints and dental sealants. Taurine is a semi-essential amino acid with antioxidant, anti-inflammatory, and anti-apoptotic actions. This study aimed to evaluate the possible protective effect of taurine on BPA-induced structural changes in the cerebral cortex of rats using histological and immunohistochemical methods. 35 Wistar rats (180-200 gm) were divided into control: 10 rats; Group I: 5 rats received corn oil (0.5 mL/day); Group II (Bisphenol low dose; BPAL): 5 rats received a low dose of BPA (25 mg/kg/three times/week); Group III (Bisphenol high dose; BPAH): 5 rats received a high dose of BPA (100 mg/kg/three times/week; Group IV: (BPAL + taurine): 5 rats received taurine 100 mg/kg/day and BPAL (25 mg/kg/three times/week); Group V: (BPAH + taurine): 5 rats received taurine 100 mg/kg/day and BPH (100 mg/kg/ three times/week). BPAL& BPAH groups showed significant dose-dependent histological changes of the neuropil, pyramidal, and neuroglial cells at H&E stained sections, significantly increased GFAP, caspase- 3 immunohistochemical reaction with cells positive for Ki67 with many mitotic figures. BPAL + taurine and BPAH + taurine groups showed amelioration of the previously mentioned results. Taurine ameliorated the structural changes induced by BPA in the cerebral cortex of rats.

Mitigating effect of ferulic acid on di-(2-ethylhexyl) phthalate-induced neurocognitive dysfunction in male rats with a comprehensive in silico survey

Di-(2-ethylhexyl) phthalate (DEHP) is the most abundant phthalate threatening public health-induced neurotoxicity. This neurotoxicity is associated with behavioral and biochemical deficits in male rats. Our study investigated the neuroprotective effect of ferulic acid (FA) on male rats exposed to DEHP. Thirty-two male Wistar rats were assigned to four groups. Group I control rats received corn oil, group II intoxicated rats received 300 mg/kg of DEHP, group III received 300 mg/kg of DEHP + 50 mg/kg of FA, and group IV received 50 mg/kg of FA, all agents administrated daily per os for 30 days. Anxiety-like behavior, spatial working memory, and recognition memory were assessed. Also, brain oxidative stress biomarkers, including brain malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide (NO), superoxide dismutase (SOD), brain-derived neurotrophic factor (BDNF) as well as heme oxygenase-1 (HO-1) were measured. Moreover, brain histopathology examinations associated with immunohistochemistry determination of brain caspase-3 were also evaluated. Furthermore, docking simulation was adapted to understand the inhibitory role of FA on caspase-3 and NO synthase. Compared to DEHP-intoxicated rats, FA-treated rats displayed improved cognitive memory associated with a reduced anxious state. Also, the redox state was maintained with increased BNDF levels. These changes were confirmed by restoring the normal architecture of brain tissue and a decrement in the immunohistochemistry caspase-3. In conclusion, FA has potent antioxidant and antiapoptotic properties that confirm the neuroprotective activity of FA, with a possible prospect for its therapeutic capabilities and nutritional supplement value.

Pentachlorophenol-induced hemotoxicity diminishes antioxidant potential and oxidizes proteins, thiols, and lipids in rat blood: An in vivo study

Pentachlorophenol (PCP) is an excessively used wood preservative and pesticide, which has resulted in human exposure raising concerns about its potential toxic effects. This study is designed to evaluate the hemotoxicity of PCP in adult rats. Wistar rats were orally administered PCP (25–150 mg/kg bw) for five days while untreated (control) rats received corn oil. Animals were sacrificed, blood was taken and fractionated into plasma and red blood cells (RBC). PCP administration increased methemoglobin formation but decreased methemoglobin reductase activity. Significantly increased hydrogen peroxide level indicates initiation of oxidative stress condition in blood. PCP increased the oxidation of thiols, proteins and lipids, lowered glutathione levels, and compromised the antioxidant status of RBC in treated rats. Enzymes of the pathways of glucose breakdown, glycolysis and phosphogluconate pathway, were inhibited. Markers of liver damage were increased in the plasma of PCP-treated rats suggesting hepatotoxicity. This was confirmed by histopathological analysis of stained liver sections. Activity of xanthine oxidase, a reactive oxygen species (ROS) generating pro-oxidant enzyme, was increased. These hematological changes could be a result of the increased generation of ROS or direct chemical transformation by transient reaction species. These results show that PCP induces redox imbalance, diminishes antioxidant potential, inhibits metabolic pathways, and oxidizes cellular components in rat blood.This study suggests an elaborated possible molecular mechanism of PCP toxicity, and similar compounds so that methods can be devised to minimize its damaging effect.

Nanocurcumin Potential Effect of SOD Enzyme and Caspase-3 Expression in Lead-Acetate Induced Rats Ovarian Granulosa Cells

Aim: This study investigated the potential effect of nanocurcumin on the increase of SOD enzyme expressionand decrease of caspase-3 in lead acetate-induced rats ovarian granulosa cells.Materials and Methods: Forty five female rats were divided into 5 groups, the negative control group (ratsreceiving corn oil, one hour later receiving distilled water), positive control group (rats receiving corn oil,one hour later receiving lead acetate of 40 mg/kg bw) and experimental groups 1, 2 and 3 (rats receivingnanocurcumin 50 mg, 100 mg and 200 mg/kg bw). One hour after administering the nanocurcumin, therats received 40 mg/kg of lead acetate. All groups received oral treatment once a day for 26 days. Onday 27 the rats were sacrificed and the expression of SOD and caspase-3 enzymes were measured usingimmunohistochemical methods.Results: This study found that lead acetate decreased SOD enzyme expression and increased caspase-3. Incontrast, nanocurcumin increased SOD enzyme and decreased caspase-3 expression in lead acetate-inducedrats ovarian granulosa cells.Conclusion: Nanocurcumin has potential as a strong natural antioxidant by affecting the increase of SODand the decrease of caspase-3 cells in lead acetate-induced rats ovarian granulosa cells.

Reproductive Toxicity Induced by Low Dose Bisphenol A(BPA) in Male Rats

Bisphenol A(BPA) an endocrine disruptor used in the manufacturing process of plastic. BPA low doses on long exposure periods had many hazardous effects.The aim of the present study was to assess the effect of lowest dose of BPA on the male induced orally on the at reproductive performance and changes in the testes that takes place histologically. P53 gene expression by Realtime PCR was also evaluated. Seventy- two albino male rats were divided into two groups, group I (control male rats receiving corn oil only). Group II (64 male rats) which was treated with oral doses of 50 µg/ kg/ day daily for 8 weeks. Every week 8 male rats were dissected and subjected to the investigated parameters. BPA treated groups presented decrease in sperms count, motility, progression and viability as well as a significant increase in sperms head or/and tail abnormalities were recognized. Histology of the testes showed abnormal and irregular organization of seminiferous tubules and decreased sperms in the testes lumen. Moreover, up-regulation in p53 expression was recorded after BPA exposure. In conclusion, these results showed that exposure to BPA at low dose 50µg/kg can cause many reproductive disorders which may impair fertility.

Protective effects of thymoquinone and diallyl sulphide against malathion-induced toxicity in rats.

Malathion is a potent organophosphate insecticide that inhibits acetylcholinesterase (AChE) enzyme. Our experimental objective was to investigate the beneficial effects of diallyl sulphide (DAS) and thymoquinone (TQ) against malathion-induced oxidative stress in rat cerebral, hepatic, and renal tissues. For 30days, rats received corn oil alone (negative control) or malathion by intragastric gavage (200mg/kg daily), either alone (positive control) or combined with oral DAS (200mg/kg daily) or TQ (10mg/kg daily) (treatment groups). Later, blood samples were collected via direct cardiac puncture and tissue samples were obtained for biochemical analysis. Malathion administration was associated with significant increases (p < 0.05) in the serum levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, γ-glutamyl transferase, cholesterol, urea, creatinine, and 8-OHdG (DNA damage biomarker), as well as significant (p < 0.05) decreases in theserum levels of total proteins, albumin, triglycerides, and AChE. Moreover, it significantly increased thetissue concentrations of malondialdehyde and nitric oxide and reduced tissue glutathione concentration and activities of antioxidant enzymes (glutathione peroxidase, superoxide dismutase, and catalase). Treatment of malathion-intoxicated rats with DAS or TQ significantly minimized these biochemical and oxidative effects with more frequent reversal to normal ranges of serum biomarkers, tissue oxidative markers, and antioxidant enzymes in the TQ group. In conclusion, treatment with DAS or TQ ameliorated the biochemical and oxidative effects of malathion, probably through reducing the generation of reactive oxygen and nitrogen radicals, as well as enhancing the antioxidant defense mechanisms.

Protective effect of Withania somnifera on nandrolone decanoate-induced biochemical alterations and hepatorenal toxicity in wistar rats

Background: Despite the beneficial effects of anabolic-androgenic steroids in the treatment of osteoporosis, hypogonadism, bone mineralization, and some muscle-wasting disorders, its misuse by athletes and non-athletes causes hepatorenal toxicity. Withania somnifera (WS) is a very important herb in Ayurveda and has adaptogenic, anticonvulsant, cytoprotective, and antioxidant properties. Objectives: The main objective of the study is to investigate the protective effect of WS also known as Ashwagandha on nandrolone decanoate (ND)-induced liver and kidney injury in Wistar rats using biochemical and histopathological assessment. Materials and Methods: Group 1 – control rats received corn oil intramuscularly, Group 2 – ND group received 16 mg/kg of ND intramuscularly, Group 3 (ND+WS100), Group 4 (ND+WS200), and Group 5 (ND+WS400) were treated with water emulsion of WS root powder (100 mg/kg, 200 mg/kg, and 400 mg/kg) along with ND (16 mg/kg). All ND treatments were given twice weekly for 4 weeks. WS was diluted in distilled water and administered orally once daily for 30 days. Liver marker enzymes alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase, total protein (TP), creatinine, and urea levels were evaluated followed by histopathological assessment of liver and kidney. Results: ND group showed elevated levels of liver enzymes, TP, creatinine, urea, and severe alterations in the hepatic and renal histology as compared with control. Drug treatments with WS to ND group considerably reversed liver marker enzymes, TP, creatinine, urea levels, and pathological damage caused to liver and renal tissue. Conclusion: The study findings reveal the protective role of WS on ND-induced hepatorenal toxicity implicating its antioxidant and therapeutic functions.

Celecoxib, a cyclooxygenase-2 inhibitor, offers chemoprevention against reproductive and neurobehavioural abnormalities induced by atrazine in male Wistar rats

The cyclooxygenase-2/prostanoid pathway (COX-2) serves as a potential therapeutic target in various pathological conditions. Thus, the modulatory effect of celecoxib (CXB), a COX-2 inhibitor, in atrazine-induced toxicity was investigated. Five groups (n = 6 rats per group) of adult male Wistar rats received corn oil (2 ml/kg), atrazine (ATZ, 300 mg/kg) and CXB (5.7 mg/kg) respectively and their combinations via the oral route. Results obtained showed reduced (p < 0.05) sperm motility (25.8%) and counts (27.6%), testosterone (29.9%), luteinizing (33%) and follicle stimulating hormones (78.7%) plus elevated total cholesterol (112.3%), triglyceride (115.7%), malondialdehyde levels respectively in ATZ-treated rats. Similarly, ATZ administration causes reduced locomotion (33.6%), spontaneous motor activity (46.6%) and catalepsy effects (157.3%) respectively. However, CXB divided doses moderately reverse reproductive abnormalities, modulate neurobehavioural deficits and slightly preserved COX-2 elevation following ATZ intoxication. Furthermore, histopathology of testis shows improvement in treated rats. Overall, our data suggest chemopreventive actions via pharmacological inhibition of COX-2 activity during ATZ toxicity.

Uterine ERα epigenetic modifications are induced by the endocrine disruptor endosulfan in female rats with impaired fertility

High ERα activity may disrupt the window of uterine receptivity, causing defective implantation. We investigated whether implantation failures prompted by endosulfan are associated with aberrant ERα uterine expression and DNA methylation status during the pre-implantation period. ERα-dependent target genes that play a crucial role in the uterine receptivity for embryo attachment and implantation were also investigated. Newborn female rats received corn oil (vehicle, Control), 6 μg/kg/d of endosulfan (Endo6) or 600 μg/kg/d of endosulfan (Endo600) on postnatal days (PND) 1, 3, 5, and 7. On PND90, females were made pregnant and on gestational day 5 (GD5, pre-implantation period) uterine samples were collected. ERα expression was assessed at protein and mRNA levels by immunohistochemistry and real time RT-PCR, respectively. ERα transcript variants mRNA containing alternative 5’-untranslated regions (5′UTRs) were also evaluated. We searched for predicted transcription factors binding sites in ERα regulatory regions and assessed their methylation status by Methylation-Sensitive Restriction Enzymes-PCR technique (MSRE-PCR). The expression of the ERα-dependent uterine target genes, i.e. mucin-1 (MUC-1), insulin-like growth factor-1 (IGF-1), and leukemia inhibitory factor (LIF), was assessed by real time RT-PCR. Both doses of endosulfan increased the expression of ERα and its transcript variants ERα-OS, ERα-O, ERα-OT and ERα-E1. Moreover, a decreased DNA methylation levels were detected in some ERα regulatory regions, suggesting an epigenetic up-regulation of it transcription. ERα overexpression was associated with an induction of its downstream genes, MUC-1 and IGF-1, suggesting that endosulfan might alter the uterine estrogenic pathway compromising uterine receptivity. These alterations could account, at least in part, for the endosulfan-induced implantation failures.

Environmental enrichment prevents anxiety-like behavior induced by progesterone withdrawal in two strains of rats

Stress vulnerability could influence the treatment response to anxiety associated with abrupt hormonal suppression. The present study explored the effects of different treatments on experimental anxiety induced by progesterone withdrawal (PW) in a stress-sensitive rat strain, Wistar Kyoto (WKY), in the burying behavior test (BBT). The following experimental series was conducted using independent groups of Wistar (control strain) and WKY ovariectomized rats: Experiment 1: Rats were treated for 5days with oil, a constant dose of progesterone (0.5mg/rat, s.c) or a combination of progesterone (0.5mg/rat, s.c) plus fluoxetine (10 mg/kg, i.p); on day 6, all rats were subjected to BBT. Experiment 2: Rats received corn oil or decreasing doses of progesterone (0.84, 0.67, 0.5, 0.33 and 0.17mg/rat; one dose daily); on day 6, the rats were subjected to BBT. Experiment 3: Rats were divided into two groups that were subjected to 30days of standard conditions or environmental enrichment (EE); from days 25 to 30, all rats received a fixed dose of progesterone (0.5mg/rat, s.c.) or vehicle. On day 31, the rats were tested with BBT. Results showed that PW increased anxiety in both strains, and fluoxetine prevented anxiety in WKY rats. In contrast, a gradual reduction of progesterone prevents the anxiety in Wistar but not in WKY. EE was preventive against the anxiety induced by PW in both strains of rats. Thus, the results suggest that anxiety induced by PW is prevented by EE while the anxiolytic effect of pharmacological treatments depends on stress vulnerability.

Maternal exposure to butyl paraben impairs testicular structure and sperm quality on male rats.

Parabens are hormonally active chemicals widely used as preservatives in foods and are frequently detected in human fluids and tissues. Therefore, the objective of this study was to determine the effects of maternal butyl paraben (BP) exposure on male sexual development. Pregnant Wistar rats received corn oil (control group), or BP at doses of 10, 100, or 200 mg/kg, subcutaneously, from gestational day 12 until postnatal day 21. Our results demonstrated that developmental BP exposure significantly increased the number of adult Leydig cells and the circulating concentrations of testosterone and attenuated FSH and LH concentrations at 200 mg/kg. BP exposure adversely affected spermatogenesis kinetics at doses of 10 and 200 mg/kg and provoked a decrease in the immunostaining of EsR1 and AR at 200 mg/kg. The sperm motility was impaired at the 10 mg/kg dose, and sperm head abnormalities were increased in all BP dose groups. We suggest that BP impairs testicular structure and function in the rat, affecting sperm quality. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1273-1289, 2017.

Hepatic and renal toxicological evaluations of an industrial ovotoxic chemical, 4-vinylcyclohexene diepoxide, in both sexes of Wistar rats.

4-Vinylcyclohexene diepoxide (VCD) is an industrial occupational health hazard chemical because it induces ovotoxicity in rodents. The current study investigated the impacts of VCD on selected hepatic and renal markers of oxidative stress and inflammation in both sexes of Wistar rats. Thus, male and female rats were randomly distributed into four groups of ten rats per group, and dosed orally with VCD for 28days. The control male and female groups of rats received corn oil only, while each of the three remaining groups of both sexes of rats received VCD (100, 250 and 500mg/kg BW) respectively. Thereafter, biomarkers of hepatic and renal oxidative damage, inflammation and immunohistochemical expressions of iNOS, COX-2, caspase-9 and caspase-3 were evaluated. The results revealed that VCD increased markers of liver and kidney functions, oxidative damage and inflammation, and disrupted the antioxidant homeostasis of the rats (p<0.05). Lastly, VCD enhanced the immunohistochemical expressions of iNOS, COX-2, caspase-9 and caspase-3 in the liver of the rats. Thus, our data imply that VCD induced toxicity in the liver and kidney of rats via the combined impacts of oxidative damage and inflammation.

6-Gingerol-Rich Fraction from Zingiber officinale Prevents Hematotoxicity and Oxidative Damage in Kidney and Liver of Rats Exposed to Carbendazim

ABSTRACTGinger (Zingiber officinale) is a globally marketed flavoring agent and cooking spice with a long history of human health benefits. The fungicide carbendazim (CBZ) is often detected in fruits and vegetables for human nutrition and has been reported to elicit toxic effects in different experimental animal models. The present study investigated the protective effects of 6-Gingerol-rich fraction (6-GRF) from ginger on hematotoxicity and hepatorenal damage in rats exposed to CBZ. CBZ was administered at a dose of 50 mg/kg alone or simultaneously administered with 6-GRF at 50, 100, and 200 mg/kg, whereas control rats received corn oil alone at 2 mL/kg for 14 days. Hematological examination showed that CBZ-mediated toxicity to the total white blood cell (WBC), neutrophils, lymphocytes, and platelets counts were normalized to the control values in rats cotreated with 6-GRF. Moreover, administration of CBZ significantly decreased the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione S-transferase as well as glutathione level in the livers and kidneys of rats compared with control. However, the levels of hydrogen peroxide (H2O2) and malondialdehyde were markedly elevated in kidneys and livers of CBZ-treated rats compared with control. The significant elevation in the plasma indices of renal and hepatic dysfunction in CBZ-treated rats was confirmed by light microscopy. Coadministration of 6-GRF exhibited chemoprotection against CBZ-mediated hematotoxicity, augmented antioxidant status, and prevented oxidative damage in the kidney and liver of rats.

BPA-induced DNA hypermethylation of the master mitochondrial gene PGC-1α contributes to cardiomyopathy in male rats.

Implication of environmental endocrine disruptors, such as bisphenol A (BPA), on the development of cardiopathy has been poorly investigated. The aim of the study was to investigate the effects of long-term exposure to BPA at the reference dose on the myocardium of rats, and the underlying mechanisms. Male rats received corn oil or 50 μg/kg/day of BPA since delactation. At 24 and 48 weeks (wk), cardiac function and mitochondrial function were examined. The mRNA expression and the methylation status of PCG-1α, a major regulator of mitochondrial biogenesis in cardiac muscle, were also tested. At 48 wk, BPA-exposed rats displayed cardiomyopathy, characterized by myocardium hypertrophy, cardiomyocyte enlargement, and impairment of cardiac function. At 24 wk, significantly reduced ATP production, dissipated mitochondrial membrane potential (Ψm) and declined mitochondrial respiratory complex (MRC) activity in cardiomyocytes were observed in BPA-exposed rats compared with the control rats, indicating a decrease in mitochondrial function occurs before the development of cardiomyopathy. Additionally, BPA exposure decreased the expression of PGC-1α and induced hypermethylation of PGC-1 α in heart tissue in 24- and 48-week-old rats. The change in methylation of PGC-1α was observed more pronounced in BPA-exposed rats at 48 wk. Overall, long-term BPA exposure induces cardiomyopathy in male rats, and the underlying mechanism may involve the impairment of cardiac mitochondrial function and the disturbance of methylation of PGC-1α.

In vivo genotoxicity of estragole in male F344 rats.

Estragole, a naturally occurring constituent of various herbs and spices, is a rodent liver carcinogen which requires bio-activation. To further understand the mechanisms underlying its carcinogenicity, genotoxicity was assessed in F344 rats using the comet, micronucleus (MN), and DNA adduct assays together with histopathological analysis. Oxidative damage was measured using human 8-oxoguanine-DNA-N-glycosylase (hOGG1) and EndonucleaseIII (EndoIII)-modified comet assays. Results with estragole were compared with the structurally related genotoxic carcinogen, safrole. Groups of seven-week-old male F344 rats received corn oil or corn oil containing 300, 600, or 1,000 mg/kg bw estragole and 125, 250, or 450 mg/kg bw safrole by gavage at 0, 24, and 45 hr and terminated at 48 hr. Estragole-induced dose-dependent increases in DNA damage following EndoIII or hOGG1 digestion and without enzyme treatment in liver, the cancer target organ. No DNA damage was detected in stomach, the non-target tissue for cancer. No elevation of MN was observed in reticulocytes sampled from peripheral blood. Comet assays, both without digestion or with either EndoIII or hOGG1 digestion, also detected DNA damage in the liver of safrole-dosed rats. No DNA damage was detected in stomach, nor was MN elevated in peripheral blood following dosing with safrole suggesting that, as far both safrole and estragole, oxidative damage may contribute to genotoxicity. Taken together, these results implicate multiple mechanisms of estragole genotoxicity. DNA damage arises from chemical-specific interaction and is also mediated by oxidative species.

Protective role of Lycopene against Aroclor 1254-induced changes on GLUT4 in the skeletal muscles of adult male rat

Aroclor 1254 is the commercial mixture of highly toxic environmental pollutant, polychlorinated biphenyls (PCBs). Being immensely durable, it is extensively used and widely distributed. Studies show that Aroclor 1254 causes a variety of adverse health effects through free radical generation. The present investigation was designed to check the effect of Aroclor 1254 on the glucose transporter protein, GLUT4, which plays a key role in glucose homeostasis. The protective role of lycopene against the adverse effect of Aroclor 1254 was also tested. Group 1 rats received corn oil as vehicle and served as control. Groups 2, 3, and 4 were administered with Aroclor 1254 [2 mg kg−1 body weight (b.w.) day−1] intraperitoneally for 30 days. Groups 3 and 4 received lycopene (2 and 4 mg kg−1 b.w. day−1, respectively) orally in addition to Aroclor 1254. After 30 days, animals were euthanized and the skeletal muscles were dissected to determine the following parameters: GLUT4 messenger RNA (mRNA), GLUT4 protein (both plasma membrane and cytosolic fractions), and 14C-2-deoxyglucose uptake. Though there was no change in GLUT4 mRNA and fasting plasma glucose levels, Aroclor 1254 significantly decreased the GLUT4 protein level in both the subcellular fractions of the gracilis and triceps muscles. Most important, 14C-2-deoxyglucose uptake showed a significant decrease in Aroclor 1254 alone treated rats, and Aroclor 1254 plus 4 mg lycopene supplementation treatment maintained the same at par with control. Thus, Aroclor 1254 has adverse effects on GLUT4 translocation and 14C-2-deoxyglucose uptake, and lycopene administered along with Aroclor 1254 has a protective role over it.

The Antidiabetic Effect of Garlic Oil is Associated with Ameliorated Oxidative Stress but Not Ameliorated Level of Pro-inflammatory Cytokines in Skeletal Muscle of Streptozotocin-induced Diabetic Rats

Oxidative stress and inflammatory condition has been broadly accepted being associated with the progression of diabetes. On the other hand, garlic (大蒜 dà suàn, bulb of Allium sativum) has been shown to possess both antioxidant and anti-inflammatory action in several clinical conditions. Our previous study demonstrated that treatment with garlic oil improves oral glucose tolerance and insulin tolerance and improves the insulin-stimulated utilization of glucose to synthesize glycogen in skeletal muscle in streptozotocin (STZ)-induced diabetes, in vivo and ex vivo, respectively. The aim of the present study is to investigate the antioxidant and anti-inflammatory effects of garlic oil (GO) in the skeletal muscle of diabetic rats. Rats with STZ-induced diabetes received GO (10, 50, or 100mg/kg body weight) or corn oil by gavage every other day for 3weeks. Control rats received corn oil only. GO dose-dependently improved insulin sensitivity, as assessed by the insulin tolerance test, and oral glucose tolerance. GO significantly elevated total glutathione and glutathione peroxidase activity and lowered the nitrate/nitrite content in skeletal muscle at 50 and 100mg/kg and significantly elevated glutathione reductase activity and lowered lipid peroxidation at 100mg/kg. By contrast, GO did not reverse diabetes-induced elevation of IL-1β and TNF-α in skeletal muscle at any tested dose. On the other hand, GO elevated the expression of GLUT4 in skeletal muscle along with glycogen content as observed with PAS staining. In conclusion, the antidiabetic effect of garlic oil is associated with ameliorated oxidative stress in skeletal muscle.

Oxidative stress modulates membrane bound ATPases in brain regions of PCB (Aroclor 1254) exposed rats: Protective role of α-tocopherol

Polychlorinated biphenyls (PCBs) are a class of widely dispersed and environmentally persistent organic compounds. PCBs exhibit a wide range of toxicological effects including neurotoxicity. Vitamin E (α-tocopherol) is an important lipid soluble antioxidant placed in a special region of membranes. Large amounts of energy are required to maintain the signaling activities of the cells in the central nervous system (CNS). Membrane proteins that control ion gradients across organellar and plasma membranes appear to be particularly susceptible to oxidation-induced changes. The aim of this study was to determine the protective role of vitamin E on Aroclor 1254 induced modulation in membrane bound ATPases in brain regions of rats. One group of rats received corn oil as vehicle for 30 days as control. The other group of rats were administered Aroclor 1254 at a dose of 2 mg kg −1 bw day −1 intraperitoneally for 30 days. One group of rats received vitamin E (50 mg kg −1 bw day −1) orally simultaneously with Aroclor 1254 for 30 days. After 30 days, the animals were euthanized and the brain was dissected to hypothalamus and hippocampus to determine the following parameters. Hydrogen peroxide (H 2O 2), Lipid peroxidation (LPO) and the activities of Na +K +-ATPase, Ca 2+-ATPase and Mg 2+-ATPase were determined. Reduced glutathione (GSH) level was also determined. Activities of all the enzymes were decreased while an increase in H 2O 2 and LPO were observed in selected brain regions of PCB treated animals. Simultaneous vitamin E treatment in PCB exposed animals restored all the parameters significantly. These results suggest that oxidative stress is involved in the inhibitory effect of PCB (Aroclor 1254) on membrane bound ATPases in selected brain regions. α-tocopherol acts against PCB induced neurotoxicity by decreasing oxidative stress.

PCB (Aroclor 1254) enhances oxidative damage in rat brain regions: Protective role of ascorbic acid

PCBs are one of the environmental toxicants and neurotoxic compounds which induce the production of free radicals leading to oxidative stress. Oxidative stress is a contributing factor to alteration caused in neurodegenerative processes. The ability of Vitamin C to retard oxidative processes has been recognized for many years. Therefore, the present experiment was carried out to determine the antioxidant role of ascorbate on Aroclor 1254 induced oxidative stress in brain regions of albino rats. One group of rats received corn oil as vehicle for 30 days as control. The other group of rats were administered Aroclor 1254 at a dose of 2 mg/kg bw/day intraperitoneally for 30 days. One group of rats received Vitamin C (100 mg/kg bw/day) orally simultaneously with Aroclor 1254 for 30 days. The brain was dissected to cerebral cortex (Cc), cerebellum (C) and hippocampus (H). Enzymatic and non-enzymatic antioxidants such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione- S-transferase (GST), reduced glutathione (GSH) and Vitamin C were estimated. Hydrogen peroxide (H 2O 2), lipid peroxidation (LPO) and acetylcholine esterase activity (AchE) were determined. Activities of SOD, CAT, GPx, GST, AchE and the concentration of GSH, Vitamin C were decreased while an increase in H 2O 2 and LPO were observed in brain regions of PCB treated animals. Vitamin C administration retrieved all the parameters except GST, significantly. These results suggest that PCB induces oxidative stress in rat brain by decreasing the activities of antioxidant enzymes, which can be protected by Vitamin C treatment.

Effects of garlic oil and diallyl trisulfide on glycemic control in diabetic rats

We investigated the effects of garlic oil and diallyl trisulfide on glycemic control in rats with streptozotocin-induced diabetes. Diabetic rats received by gavage garlic oil (100 mg/kg body weight), diallyl trisulfide (40 mg/kg body weight), or corn oil every other day for 3 weeks. Control rats received corn oil only. Both garlic compounds significantly raised the basal insulin concentration. The insulin resistance index as assessed by homeostasis model assessment and the first-order rate constant for glucose disappearance were significantly improved by both garlic compounds ( P < 0.05). Oral glucose tolerance was also improved by both garlic compounds and was accompanied by a significantly increased rate of insulin secretion ( P < 0.05). Glycogen formation (but not that of lactate or carbon dioxide) from glucose by the soleus muscle in the presence of 10 or 100 μU/ml of insulin was significantly better after treatment with both garlic compounds. Both garlic oil and diallyl trisulfide improve glycemic control in diabetic rats through increased insulin secretion and increased insulin sensitivity.