Vaccine Side Effects Following COVID-19 Vaccination Among the Residents of the UAE-An Observational Study.

COVID-19 vaccines have proven to be very safe in the clinical trials, however, there is less evidence comparing the safety of these vaccines in real-world settings. Therefore, we aim to investigate the nature and severity of the adverse effects reported and the differences based on the type of vaccine received. A survey was conducted among 1,878 adult (≥18 years) COVID-19 vaccine recipients through online survey platforms and telephonic interviews during March to September 2021. The factors potentially associated with the reported side effects like age, gender, ethnicity, comorbidities, and previous COVID-19 infection were analyzed based on the type of vaccine received. Differences in adverse events and the severity were compared between inactivated and mRNA vaccine recipients. The major adverse effects reported by the COVID-19 vaccine recipients were pain at the site of injection, fatigue and drowsiness, and headache followed by joint/muscle pain. The adverse effects were more common among recipients of mRNA Pfizer-BioNTech vaccine than among recipients of inactive Sinopharm vaccine with the odds ratio of 1.39 (95% CI 1.14-1.68). The average number of adverse effects reported between individuals who had received Sinopharm and Pfizer-BioNTech vaccines was 1.61 ± 2.08 and 2.20 ± 2.58, respectively, and the difference was statistically significant (p <0.001). Severe adverse effects after COVID-19 vaccinations were rare and 95% of the adverse effects reported after either an inactivated or mRNA vaccine were mild requiring no or home-based treatment. The study found that individuals less than 55 years of age, female gender, with history of one or more comorbid conditions, who had received mRNA Pfizer- BioNTech vaccine, and with history of COVID-19 infections are at higher odds of developing an adverse effect post COVID-19 vaccination compared to the others.

Conserved spinal cord bioenergetics in experimental autoimmune encephalomyelitis in C57BL6 mice, measured using phosphorescence oxygen analyzer.

BACKGROUND: We have previously reported that spinal cord respiration (cellular mitochondrial oxygen consumption) and ATP content are conserved in the studied model of experimental autoimmune encephalomyelitis (EAE), foreseeing a recovery of the diseased rats. This exemplary lesion of multiple sclerosis is used here to measure spinal cord bioenergetics in C57BL6 mice. Our hypothesis is that, despite the well-known focal axonal mitochondrial pathology, bioenergetics of the CNS is reasonably preserved in this disease. METHODS: EAE was induced with an immunodominant myelin oligodendrocyte glycoprotein epitope in complete Freund's adjuvant, appended by injections of pertussis toxin. A low- and high-dose of the encephalitogen, administered into base of tail or hind-flank, were investigated. Control mice received only the incomplete adjuvant into tail. Oxygen measurements were based on quenching the phosphorescence of Pd(II) meso-tetra (sulfophenyl) tetrabenzoporphyrin by molecular oxygen. Cellular ATP was measured using the luciferin/luciferase system. RESULTS: The kinetics of spinal cord oxygen consumption was zero-order (linear with time) and inhibited by cyanide, confirming oxygen was reduced by cytochrome oxidase. The rate of respiration (in µM O2.min-1.mg-1; measured on Days 13-28) in control mice was (mean ± SD) 0.086 ± 0.024 (n = 8) and in immunized mice was 0.079 ± 0.020 (n = 15, P = 0.265, Mann-Whitney test). Consistently, cellular ATP (in µmol mg-1 dry pellet weight; measured on Days 13-28) in control mice was 0.068 ± 0.079 (n = 11) and in immunized mice was 0.063 ± 0.061 (n = 24, P = 0.887, Mann-Whitney U test). CONCLUSIONS: In vitro measurements of spinal cord bioenergetics show conservation of the mitochondrial function in mice with EAE. These results suggest the previously documented reduced mitochondrial electrochemical potential in this disease is alterable, and likely reflects the adverse events of neuroinflammation.

The use of phosphorescence oxygen analyzer to measure the effects of rotenone and 1-methyl-4-phenylpyridinium on striatal cellular respiration in C57BL6 mice.

BACKGROUND: We have previously reported on the use of the phosphorescence oxygen analyzer for measuring spinal cord cellular respiration. This analytical tool is used here to investigate the effects of two inhibitors of NADH:ubiquinone oxidoreductase, rotenone and 1-methyl-4-phenylpyridinium, on cellular respiration in striatal tissue. Both neurotoxins can induce Parkinson's disease-like symptoms, and have been used to study this disease in animals. Our hypothesis is that striatal cellular respiration is a sensitive biomarker for the adverse effects of toxins, and the phosphorescence oxygen analyzer can be used as a screening tool for this purpose. METHODS: Striatal fragments were collected from C57BL6 mice and immersed in Pd phosphor solution [phosphate-buffered saline, 3.0 µM 'Pd(II)-meso-tetra (sulfophenyl) tetrabenzoporphyrin' and 0.5% fat-free albumin, with and without 5.0 mM glucose]. The sample was transferred to a glass vial containing 2-mL Pd phosphor solution. The vial was sealed from air and placed in the instrument that measures dissolved oxygen as function of time. Immunoblots of the studied tissue were positive for the dopamine neuronal cell biomarker tyrosine hydroxylase. RESULTS: Striatal oxygen consumption was linear with time, exhibiting zero-order kinetics of oxygen reduction by cytochrome oxidase. Cyanide sensitive respiration was ≥90%, confirming oxygen was reduced by cytochrome oxidase. The rate of respiration increased by ~2-fold in the presence of glucose. Striatal oxygen consumption in the presence of rotenone or 1-methyl-4-phenylpyridinium was exponential, demonstrating impaired respiration. CONCLUSION: Striatal cellular mitochondrial oxygen consumption was impaired by the studied inhibitors of complex I of the respiratory chain. This effect is expected to deplete NAD+ (oxidized nicotinamide adenine dinucleotide), a principle driver of glycolysis. In vivo studies are required to determine if these toxin-induced metabolic derangements contribute to the development of sporadic Parkinson's disease. This analytic tool can be used to screen environmental toxins for their in vitro effects on the striatum.

Child maltreatment and neglect in the United Arab Emirates and relationship with low self-esteem and symptoms of depression.

OBJECTIVES: To our knowledge, this study is the first in the United Arab Emirates (UAE) to investigate the prevalence of child maltreatment in relation to depressive symptoms and self-esteem. STUDY DESIGN: Exposure to physical maltreatment, emotional abuse and neglect was evaluated in 518 adolescents (86% response rate) randomly selected from schools in Al Ain in the Emirate of Abu Dhabi. The Rosenberg self-esteem scale and the Beck Depression Inventory were used to measure self-esteem and depressive symptoms by using multivariate logistic regression analyses. RESULTS: The mean age of study participants was 14.3 years. Emotional abuse was the most frequent form of maltreatment (33.9%), physical abuse (12.6%) and neglect (12.1%) followed. Male sex was a positive predictor of physical abuse (OR = 2.12; 95% CI 1.18-3.77), whilst higher maternal level of education was protective (OR = 0.40; 95% CI 0.19-0.86). Daily screen time (OR = 2.77; 95% CI 1.17-6.56) and tobacco smoking (OR = 1.86; 95% CI 1.09-3.18) positively predicted emotional abuse. Emotionally maltreated and neglected participants were less likely to report high level of self-esteem and more likely to report symptoms of depression. CONCLUSIONS: Child maltreatment in the UAE is of a similar magnitude to what reported in other countries around the world and significantly associated with low self-esteem and depressive symptoms.

Dose-related biphasic effect of the Parkinson's disease neurotoxin MPTP, on the spread, accumulation, and toxicity of α-synuclein.

BACKGROUND: Parkinson's disease (PD), the second most common progressive neurodegenerative disorder, is characterized by the abnormal accumulation of intraneuronal inclusions enriched in aggregated α-synuclein (α-syn), known as Lewy bodies (LBs) and Lewy neurites (LNs), and significant loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc) of the brain. Recent evidence suggests that the intrastriatal inoculation of α-syn preformed fibrils (PFF) in mice brain triggers endogenous α-syn in interconnected brain regions. 1-methyl, 4-phenyl, 1,2,3,6 tetrahydropyridine (MPTP), a mitochondrial neurotoxin, has been used previously to generate a PD mouse model. However, the common methods of MPTP exposure do not induce LB or α-syn aggregation in mice. In the present study, we evaluated the effect of different doses of MPTP (10 mg/kg.b.wt and/or 25 mg/kg.b.wt) on the spread, accumulation, and toxicity of endogenous α-syn in mice administered an intrastriatal injection of human α-syn PFF. METHODS: We inoculated human WT α-syn PFF in mouse striatum. At 6 weeks post PFF injection, we challenged the animal with two different doses of MPTP (10 mg/kg.b.wt and 25 mg/kg.b.wt) once daily for five consecutive days. At 2 weeks from the start of the MPTP regimen, we collected the mice brain and performed immunohistochemical analysis, and Rotarod test to assess motor coordination and muscle strength before and after MPTP injection. RESULTS: A single injection of human WT α-syn PFF in the mice striatum induced the propagation of α-syn, occurring as phosphorylated α-synuclein (pS129), towards the SNpc, within a very short time. Injection of a low dose of MPTP (10 mg/kg.b.wt) at 6 weeks post α-syn PFF inoculation further enhanced the spread, whereas a high dose of MPTP (25 mg/kg.b.wt.) reduced the spread. Majority of the accumulated α-syn were proteinase K resistant, as recognized using a conformation-specific α-syn antibody. Injection of α-syn PFF alone caused 12 % reduction in the number of tyrosine hydroxylase positive neurons while α-syn PFF + a low dose of MPTP caused 33 % reduction (loss), compared to the control mice injected with saline. This combination also reduced the motor coordination. Interestingly, a low dose of MPTP alone did not cause any significant reduction in the number of tyrosine hydroxylase positive neurons compared to saline treatment. Animals that received α-syn PFF and a high dose of MPTP showed massive activation of glial cells and decreased spread of α-syn, majority of which were detected in the nucleus. CONCLUSION: Our results suggest that a combination of human WT α-syn PFF and a low dose of MPTP increases the pathological conversion and propagation of endogenous α-syn, and neurodegeneration, within a very short time. Our model can be used to study the mechanisms of α-syn propagation and screen for potential drugs against PD.

Exercise protects against insulin-dependent diabetes-induced osteoarthritis in rats: A scanning electron microscopy study.

We tested the hypothesis that swim exercise can protect the articular cartilage from damages induced secondary to insulin-dependent diabetes mellitus in rats using the scanning electron microscopy and to monitor the blood levels of oxidative and antioxidative stress biomarkers that are known to be modulated in osteoarthritis (OA). A profound damage to the cartilage was observed in the diabetic rats. Our findings also show that swim exercise protects the knee joints from damage induced by diabetes as well as significantly inhibiting OA-induced upregulation of thiobarbituric acid reactive substances (TBARS) and tumor necrosis factor alpha (TNF-α) and augmented superoxide dismutase (SOD) inhibition by OA. Thus, we demonstrated an effective protection by swim exercise against diabetes-induced OA in a rat model of the disease.

Bioenergetics of the spinal cord in experimental autoimmune encephalitis of rats.

BACKGROUND: Mitochondrial dysregulation is important in axonal damage and demyelination in multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE). There is however, no evidence in the literature of any study that has examined cellular bioenergetics of the central nervous system (CNS) during the early development and clinical course of EAE. EAE, a rodent model of relapsing/remitting MS, is a CD4(+) T cell-mediated disease of the CNS. We hypothesize that CNS bioenergetics might predict prognosis, and that preserved bioenergetics might underlie the remission from disease. The study aims therefore, to determine whether the clinical history of EAE is influenced by cellular respiration of the CNS in susceptible Dark Agouti (DA) and resistant Albino Oxford (AO) rats. METHODS: Experimental autoimmune encephalomyelitis was induced by myelin basic protein in complete Freud Adjuvant in the footpads of DA and AO rats. A phosphorescence analyzer that determines cellular respiration was used to monitor oxygen consumption and ATP concentration was measured using the Enliten ATP assay system. Disease pathology was demonstrated by H&E and Luxol fast blue staining of sections of the lumbar regions of the spinal cord. Mitochondrial size in relation to axonal size was determined by electron microscopy. Apoptosis was studied by HPLC measurement of intracellular caspase-3 activity and caspase immunohistochemistry. Role and source of caspase 1 was studied by double immunofluorescence with antibodies for caspase-1, microglia (anti-Iba1) and astrocytes (anti-GFAP). RESULTS: The cellular respiration of the CNS did not vary between diseased and normal rats. We also demonstrate here, that at the peak of disease, inflammation as shown by caspase-1, produced by activated microglia and infiltrating cells, was significant in susceptible DA rats. The mitochondrial:axonal size ratio did not vary in the different groups although mitochondria were smaller in spinal cords of diseased DA rats. Demyelination, observed only in areas of mononuclear infiltration of the spinal cord of diseased DA rats, was demonstrated by light microscopy and electron microscopy. CONCLUSION: We conclude that EAE at this early stage does not significantly affect CNS cellular respiration and this might underlie the reason for the recovery of diseased rats.

Students' perspectives on promoting healthful food choices from campus vending machines: a qualitative interview study.

BACKGROUND: Increasing the healthfulness of campus food environments is an important step in promoting healthful food choices among college students. This study explored university students' suggestions on promoting healthful food choices from campus vending machines. It also examined factors influencing students' food choices from vending machines. METHODS: Peer-led semi-structured individual interviews were conducted with 43 undergraduate students (33 females and 10 males) recruited from students enrolled in an introductory nutrition course in a large national university in the United Arab Emirates. Interviews were audiotaped, transcribed, and coded to generate themes using N-Vivo software. RESULTS: Accessibility, peer influence, and busy schedules were the main factors influencing students' food choices from campus vending machines. Participants expressed the need to improve the nutritional quality of the food items sold in the campus vending machines. Recommendations for students' nutrition educational activities included placing nutrition tips on or beside the vending machines and using active learning methods, such as competitions on nutrition knowledge. CONCLUSIONS: The results of this study have useful applications in improving the campus food environment and nutrition education opportunities at the university to assist students in making healthful food choices.

The cytotoxicity of aflatoxin b1 in human lymphocytes.

OBJECTIVES: Aflatoxin B1 (AFB1) is a naturally occurring carcinogenic and immunosuppressive compound. This study was designed to measure its toxic effects on human peripheral blood mononuclear cells (PBMC). METHODS: The study recruited 7 healthy volunteers. PBMC were isolated and cellular respiration was monitored using a phosphorescence oxygen analyser. The intracellular caspase activity was measured by the caspase-3 substrate N-acetyl-asp-glu-val-asp-7-amino-4-methylcoumarin. Phosphatidylserine exposure and membrane permeability to propidium iodide (PI) were measured by flow cytometry. RESULTS: Cellular oxygen consumption was inhibited by 2.5 µM and 25 µM of AFB1. Intracellular caspase activity was noted after two hours of incubation with 100 µM of AFB1. The number of Annexin V-positive cells increased as a function of AFB1 concentration and incubation time. At 50 µM, a significant number of cells became necrotic after 24 hours (Annexin V-positive and PI-positive). CONCLUSION: The results show AFB1 is toxic to human lymphocytes and that its cytotoxicity is mediated by apoptosis and necrosis.

Pam3CSK(4) enhanced beta cell loss and diabetogenesis: the roles of IFN-gamma and IL-17.

Toll like receptors are primary sensors of both innate and adaptive immune systems. They activate APCs and influence T-cell function in inflammatory autoimmune response. Studies have shown that TLR manipulation may lead to either tolerance or trigger autoimmunity. Using diabetogenic and subdiabetogenic multiple low doses of streptozotocin, we demonstrate here that Pam3 CYS-CK4 a TLR-2 agonist, enhances and promotes diabetes in C57BL/6 male mice following increased apoptosis of ß islet cells. FACS analysis of isolated pancreatic lymph node cells revealed significant increased number of macrophages, dendritic cells, CD4(+) TNF-α(+), CD4(+) IFN-γ(+) and most significantly, CD4(+) IL-17(+) and reduced number of CD25(+)Fox p3(+) T cells after Pam3CSK4 treatment. Genetic deletion of IFN-γ prevents whereas deletion of IL-17 reduced severity of Pam3CSK4-induced enhancement of diabetes. TLR-2 agonist-enhanced diabetogenesis is also influenced by enhanced influx of antigen presenting cells and suppression of regulatory T cell activity.

Derangements of liver tissue bioenergetics in concanavalin A-induced hepatitis.

BACKGROUND: A novel in vitro system was employed to investigate liver tissue respiration (mitochondrial O2 consumption) in mice treated with concanavalin A (Con A). This study aimed to investigate hepatocyte bioenergetics in this well-studied hepatitis model. METHODS: C57Bl/6 and C57Bl/6 IFN-γ-/- mice were injected intravenously with 12 mg ConA/kg. Liver specimens were collected at various timepoints after injection and analyzed for cellular respiration and caspase activation. Serum was analyzed for interferon-gamma (IFN-γ) and aminotransferases. Fluorescence activated cell sorting analysis was used to determine the phenotype of infiltrating cells, and light and electron microscopy were used to monitor morphological changes. Phosphorescence analyzer that measured dissolved O2 as function of time was used to evaluate respiration. RESULTS: In sealed vials, O2 concentrations in solutions containing liver specimen and glucose declined linearly with time, confirming zero-order kinetics of hepatocyte respiration. O2 consumption was inhibited by cyanide, confirming the oxidation occurred in the respiratory chain. Enhanced liver respiration (by ≈68%, p<0.02) was noted 3 hr after ConA treatment, and occurred in conjunction with limited cellular infiltrations around the blood vessels. Diminished respiration (by ≈30%, p=0.005) was noted 12 hr after ConA treatment, and occurred in conjunction with deranged mitochondria, areas of necrosis, and prominent infiltrations with immune cells, most significantly, CD3+NKT+ cells. Increases in intracellular caspase activity and serum IFN-γ and aminotransferase levels were noted 3 hr after ConA treatment and progressed with time. The above-noted changes were less pronounced in C57Bl/6 IFN-γ-/- mice treated with ConA. CONCLUSIONS: Based on these results, liver tissue bioenergetics is increased 3 hr after ConA exposure. This effect is driven by the pathogenesis of the disease, in which IFN-γ and other cytokines contribute to. Subsequent declines in liver bioenergetics appear to be a result of necrosis and active caspases targeting the mitochondria within hepatocytes.

IFN-γ deficiency exacerbates experimental autoimmune neuritis in mice despite a mitigated systemic Th1 immune response.

Previous studies have shown that interferon-gamma (IFN-γ) is a proinflammatory cytokine that contributes to the pathogenesis of Guillain-Barré syndrome and its animal model, experimental autoimmune neuritis (EAN). Treatments with anti-IFN-γ antibodies improve clinical outcome in GBS patients and EAN animals and administration of IFN-γ markedly worsens EAN. Paradoxically, the mice deficient in IFN-γ remain susceptible to experimental autoimmune encephalomyelitis, an analogous disease in the central nervous system. These observations raise a question whether IFN-γ might be protective in autoimmune demyelinating diseases. To clarify the role of IFN-γ in the pathogenesis of autoimmune demyelinating diseases, we used P0 protein peptide 180-199 to induce EAN in IFN-γ knockout (KO) mice. After the acute phase of EAN, the clinical signs of IFN-γ KO mice were significantly more severe than those of wild type (WT) controls. After antigenic stimulation, the proliferation of splenic mononuclear cells was significantly higher in IFN-γ KO than in WT mice with EAN. At the peak of EAN, the proportion of interleukin (IL)-17A expressing cells in cauda equina (CE) infiltrating cells, and the levels of IL-17A in sera were elevated in IFN-γ KO mice when compared with their WT counterparts. The proportions of major histocompatibility complex (MHC) II, macrosialin, and IL-12/IL-23p40 expressing cells, relative to total CE infiltrating cells were correspondingly higher in IFN-γ KO than in WT mice with EAN. However, IFN-γ deficiency reduced the production of NO by cultured macrophages in response to proinflammatory stimuli and induced a systemic Th2-oriented immune response. In conclusion, IFN-γ deficiency exacerbates EAN via upregulating Th17 cells despite a mitigated systemic Th1 immune response.

Use of antimicrobial agents in food processing systems.

This article reviews the patents showing the use of antimicrobial agents in processing plants to eliminate the growth of the microorganism that affects on the quality and safety of the end products. Several materials have unique antimicrobial effects, especially towards biofilms in the processing equipments. The selection of a proper antimicrobial agent is essential to obtain the best results in preserving foods. The antimicrobial agent must not be toxic, and many factors need to be considered in choosing the right antimicrobial agent.

Carbon monoxide poisoning in the United Arab Emirates.

Carbon monoxide (CO) poisoning is rare in the Arabian Peninsula and occurs almost exclusively during the winter months. Knowledge and perception of the hazards of carbon monoxide is limited. Migrant workers from warm climates appear particularly at risk. We investigated 46 cases of carbon monoxide poisoning presenting at emergency departments from 2007-2009 of the two main hospitals in Al Ain city, United Arab Emirates. Interviews, hospital records, and administered questionnaires were used to collect the data. Among the 46 cases investigated, 24 (52%) were males. Foreign nationals compromised 80% of the cases and the incidence was 3.1 cases per 100,000 residents per year. Burning charcoal in poorly ventilated residences was the predominant source of the carbon monoxide poisoning. Almost all cases (98%) were admitted during the winter months, most in the early morning hours. Carboxyhaemoglobin (COHb) was significantly increased in cases with loss of consciousness and depressed consciousness. There were no reported fatalities.

Measurement of oxygen consumption by murine tissues in vitro.

INTRODUCTION: A novel in vitro system was developed to measure O2 consumption by murine tissues over several hours. METHODS: Tissue specimens (7-35 mg) excised from male Balb/c mice were immediately immersed in ice-cold Krebs-Henseleit buffer, saturated with 95% O2:5% CO2. The specimens were incubated at 37 °C in the buffer, continuously gassed with O2:CO2 (95:5). [O2] was determined as a function of time from the phosphorescence decay rates (1/τ) of Pd(II) meso-tetra-(4-sulfonatophenyl)-tetrabenzoporphyrin. The values of 1/τ were linear with [O2]: 1/τ=1/τo + kq [O2]; 1/τo=the decay rate for zero O2, kq=the rate constant in s⁻¹ µM⁻¹. RESULTS: NaCN inhibited O2 consumption, confirming oxidation occurred in the mitochondrial respiratory chain. The rate of respiration in lung specimens incubated in vitro for 3.9≤t≤12.4 h was 0.24±0.03 µM O2 min⁻¹ mg⁻¹ (mean±SD, n=28). The corresponding rate for the liver was 0.27±0.13 (n=11, t≤4.7 h), spleen 0.28± 0.07 (n=10, t≤5h), kidney 0.34±0.12 (n=7, t≤5h) and pancreas 0.35±0.09 (n=10, t≤4h). Normal tissue histology at hour 5 was confirmed by light and electron microscopy. There was negligible number of apoptotic cells by caspase 3 staining. DISCUSSION: This approach allows accurate assessment of tissue bioenergetics in vitro.

Biocompatibility of calcined mesoporous silica particles with cellular bioenergetics in murine tissues.

A novel in vitro system was developed to investigate the effects of two forms of calcined mesoporous silica particles (MCM41-cal and SBA15-cal) on cellular respiration of mouse tissues. O(2) consumption by lung, liver, kidney, spleen, and pancreatic tissues was unaffected by exposure to 200 µg/mL MCM41-cal or SBA15-cal for several hours. Normal tissue histology was confirmed by light microscopy. Intracellular accumulation of the particles in the studied tissues was evident by electron microscopy. The results show reasonable in vitro biocompatibility of the mesoporous silicas with murine tissue bioenergetics.

Effect of vitamin C on liver and kidney functions in normal and diabetic rats.

Diabetes mellitus (DM) is recognized as one of the leading causes of morbidity and mortality in the world. About 5-6% of the world population suffers from this disease and the number of people diagnosed with diabetes is rapidly increasing. Diabetes has been demonstrated to be associated with oxidative stress and hyperglycemia, one of the most important indicators of oxidative stress. The endogenous mechanisms of enzymes and antioxidants are able to destroy the reactive species and create a balance between antioxidant and free radicals. In diabetes, the oxidative stress is increased because of the deficiency in the antioxidant defense. The intake of antioxidants, such as vitamin C, may reduce the oxidative stress associated with diabetes and hence help to restore the antioxidant defense system. The aim of this article was to investigate the effect of different doses of vitamin C on the biochemical parameters of normal and streptozotocin (STZ)-induced diabetic rats. Biochemical analysis was used to study the effect of this vitamin on the biochemical parameters of normal and diabetic rats. Liver and kidney enzymes were elevated after the onset of diabetes. Moderate doses of vitamin C significantly (P < 0.0008) reduced plasma gamma-glutamyl level in diabetic rats. Moreover, vitamin C significantly (P < 0.01) reduced the blood urea nitrogen level of diabetic rats. The plasma level of electrolytes, such as calcium and sodium, also changed significantly (P < 0.00001) after oral administration of vitamin C. Antioxidants, such as vitamin C, may ameliorate the biochemical parameters of diabetic rats.

Vitamin E ameliorates some biochemical parameters in normal and diabetic rats.

Diabetes is associated with hyperglycemia, one of the most important causes of oxidative stress. Endogenous antioxidants are able to destroy the reactive species and create a balance between antioxidant and free radicals. In diabetes, the oxidative stress is increased due to the deficiency in the antioxidant defense. The intake of antioxidants, such as vitamin E, may reduce the oxidative stress associated with diabetes and hence help to restore the antioxidant defense system. The aim of this article was to investigate the effect of different doses of vitamin E on the biochemical parameters of normal and streptozotocin (STZ)-induced diabetic rats. Biochemical analysis was used to study the effect of this vitamin on the biochemical parameters of normal and diabetic rats. The plasma levels of alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactic dehydrogenase (LDH), and gamma-glutamyl transferase (gamma-GT) were significantly increased after the onset of diabetes. In addition, STZ-induced diabetes also caused an increase in the level of blood urea nitrogen (BUN) and creatinine. Oral administration of vitamin E (0.2-0.4 mg daily) significantly (P < 0.05) decreased the plasma level of ALT, AST, and gamma-GT. In addition, there was a slight but not significant reduction in the plasma level of ALP. Parameters of kidney function, such as BUN and creatinine, were slightly reduced after the oral administration of vitamin E. The plasma level of electrolytes, such as calcium and sodium, also changed significantly (P < 0.00001) after the oral administration of vitamin E. Vitamin E ameliorates the metabolic and biochemical parameters of diabetic rats.

Vitamin E decreases the hyperglucagonemia of diabetic rats.

Vitamin E has the ability to scavenge a wide spectrum of free radicals, including singlet oxygen, superoxide, and hydroxyl radicals. It has beneficial effects against several other disorders, such as atherosclerosis and ischemic heart disease, because it acts as a transcriptional regulator for gene expression via a transcription factor TAP. The beneficial effect of vitamin E on plasma insulin and glucagon levels was examined using radioimmunoassay technique. Diabetes was induced in rats by a single intraperitoneal injection of streptozotocin at a dose of 60 mg/kg body weight. Vitamin E was given at a dose of either 0.2 mg, 0.4 mg, or 0.8 mg per animal 10 days before and after the onset of diabetes. Vitamin E significantly (P < 0.05) increased plasma insulin levels in normal rats but failed to increase the plasma insulin level in diabetic rats. In contrast, vitamin E caused a significant (P < 0.05) reduction in plasma glucagon level in rats treated before and after the onset of diabetes. Vitamin E may ameliorate some diabetic complication via reduction in the level of circulating glucagon.