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1.
Bratisl Lek Listy ; 122(10): 732-738, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34570575

RESUMO

BACKGROUND: The use of acetaminophen (APAP) is increasing recently, especially with COVID-19 outbreaks. APAP is safe at therapeutic levels, however, an overdose can cause severe liver injury. This study aims to explore possible mechanisms involved in APAP­induced hepatotoxicity and compare different hepatoprotective agents, namely vitamin E, hydrogen sulfide (H2S) and necrostatin-1 (NEC-1). METHODS: Adult male albino rats were divided into groups: Control group, APAP­induced hepatotoxicity group, Vitamin E­treated group, H2S­treated group and NEC-1­treated group. Serum levels for aspartate aminotransferase (AST), alanine aminotransferase (ALT), interleukin-33 (IL-33), tumor necrosis factor alpha (TNF-α), reduced glutathione (GSH) and lipid profile were measured. Histopathological examinations of liver tissue with H(et)E stain and immunohistochemistry for activated caspase-3 were also done. RESULTS: APAP­treated group showed elevated liver transaminases, hyperlipidemia, and deficient liver anti-oxidative response together with disturbed hepatic architecture and increased immune-expression of activated caspase-3 in hepatic tissue. Pretreatment with vitamin E, H2S or NEC-1 reversed the affected parameters. Vitamin E and H2S showed greater improvement when compared to NEC-1. CONCLUSION: Vitamin E, H2S and NEC-1 showed protective effects against APAP-induced hepatotoxicity, thus they may be used as an adjuvant therapy when APAP is indicated for long periods as is the case in COVID-19 patients (Tab. 2, Fig. 2, Ref. 45). Text in PDF www.elis.sk Keywords: acetaminophen, hepatotoxicity, apoptosis, necrostatin-1, vitamin E, H2S.


Assuntos
COVID-19 , Doença Hepática Induzida por Substâncias e Drogas , Sulfeto de Hidrogênio , Acetaminofen/toxicidade , Alanina Transaminase/metabolismo , Animais , Aspartato Aminotransferases/metabolismo , Doença Hepática Induzida por Substâncias e Drogas/tratamento farmacológico , Doença Hepática Induzida por Substâncias e Drogas/metabolismo , Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle , Humanos , Sulfeto de Hidrogênio/metabolismo , Imidazóis , Indóis , Fígado/metabolismo , Masculino , Estresse Oxidativo , Ratos , SARS-CoV-2 , Vitamina E/farmacologia
2.
Free Radic Biol Med ; 175: 121-129, 2021 11 01.
Artigo em Inglês | MEDLINE | ID: mdl-34481936

RESUMO

Vitamin E, a generic term for tocopherol (T) and tocotrienol (T3), is one of the most potent lipid-soluble antioxidants in the body. It is classified into T and T3 based on the difference in the side chain structure. T and T3 have four isoforms: α-, ß-, γ-, and δ, which have different chroman rings. Both T and T3 exhibit a similar ability to scavenge free radicals, and the extent of this ability depends on the difference in the chroman structure. However, they display unique cytoprotective activities in cultured cells depending on the difference in the side chain structure. The cytoprotective effects of vitamin E have received much attention in the prevention of ferroptosis, which is a distinct form of cell death involving iron-dependent lipid peroxidation. This review focuses on the cytoprotective actions of vitamin E isoforms against oxidative stress, particularly the difference between T and T3 and its relation to cellular uptake and distribution. Moreover, the molecular mechanism for cytoprotection of vitamin E oxidation products is explained, and the complementary role of vitamin E and selenoproteins to prevent lipid peroxidation and ferroptosis is described. Furthermore, the evaluation of vitamin E's radical scavenging activity in vivo using oxidative stress markers is discussed, particularly based on kinetic data and the physiological molar ratio of vitamin E to substrates, and the limited role of vitamin E as a peroxyl radical scavenger is described. The future directions and unresolved issues related to vitamin E and lipid peroxidation are also discussed.


Assuntos
Peróxidos , Vitamina E , Antioxidantes/farmacologia , Sequestradores de Radicais Livres/farmacologia , Peroxidação de Lipídeos , Isoformas de Proteínas/genética , Selenoproteínas , Vitamina E/farmacologia
3.
Nutrients ; 13(7)2021 Jul 10.
Artigo em Inglês | MEDLINE | ID: mdl-34371875

RESUMO

Polycyclic aromatic hydrocarbons (PAHs) have been recognized to cause neurobehavioral dysfunctions and disorder of cognition and behavioral patterns in childhood. Momordica charantia L. (MC) has been widely known for its nutraceutical and health-promoting properties. To date, the effect of MC for the prevention and handling of PAHs-induced neurotoxicity has not been reported. In the current study, the neuroprotective effects of MC and its underlying mechanisms were investigated in mouse hippocampal neuronal cell line (HT22); moreover, in silico analysis was performed with the phytochemicals MC to decipher their potential function as neuroprotectants. MC was demonstrated to possess neuroprotective effect by reducing reactive oxygen species' (ROS') production and down-regulating cyclin D1, p53, and p38 mitogen-activated protein kinase (MAPK) protein expressions, resulting in the inhibition of cell apoptosis and the normalization of cell cycle progression. Additionally, 28 phytochemicals of MC and their competence on inhibiting cytochrome P450 (CYP: CYP1A1, CYP1A2, and CYP1B1) functions were resolved. In silico analysis of vitamin E and stigmasterol revealed that their binding to either CYP1A1 or CYP1A2 was more efficient than the binding of each positive control (alizarin or purpurin). Together, MC is potentially an interesting neuroprotectant including vitamin E and stigmasterol as probable active components for the prevention for PAHs-induced neurotoxicity.


Assuntos
Hipocampo/efeitos dos fármacos , Momordica charantia , Neurônios/efeitos dos fármacos , Fármacos Neuroprotetores/farmacologia , Extratos Vegetais/farmacologia , Hidrocarbonetos Policíclicos Aromáticos/toxicidade , Estigmasterol/farmacologia , Vitamina E/farmacologia , Animais , Apoptose/efeitos dos fármacos , Proteínas Reguladoras de Apoptose/metabolismo , Ciclo Celular/efeitos dos fármacos , Proteínas de Ciclo Celular/metabolismo , Linhagem Celular , Citocromo P-450 CYP1A1/metabolismo , Citocromo P-450 CYP1A2/metabolismo , Hipocampo/metabolismo , Hipocampo/patologia , Camundongos , Momordica charantia/química , Neurônios/metabolismo , Neurônios/patologia , Estresse Oxidativo/efeitos dos fármacos , Extratos Vegetais/isolamento & purificação , Ligação Proteica , Espécies Reativas de Oxigênio/metabolismo , Estigmasterol/isolamento & purificação , Vitamina E/isolamento & purificação
4.
Molecules ; 26(15)2021 Jul 27.
Artigo em Inglês | MEDLINE | ID: mdl-34361674

RESUMO

(1) Background: the current research was conducted to investigate the potential non-antioxidant roles of vitamin E in the protection of hepatocysts from oxidative damage. (2) Methods: primary sheep hepatocytes were cultured and exposed to 200, 400, 600, or 800 µmol/L hydrogen peroxide, while their viability was assessed using a CCK-8 kit. Then, cells were treated with 400 µmol/L hydrogen peroxide following a pretreatment with 50, 100, 200, 400, and 800 µmol/L vitamin E and their intracellular ROS levels were determined by means of the DCF-DA assay. RNA-seq, verified by qRT-PCR, was conducted thereafter: non-treated control (C1); cells treated with 400 µmol/L hydrogen peroxide (C2); and C2 plus a pretreatment with 100 µmol/L vitamin E (T1). (3) Results: the 200-800 µmol/L hydrogen peroxide caused significant cell death, while 50, 100, and 200 µmol/L vitamin E pretreatment significantly improved the survival rate of hepatocytes. ROS content in the cells pretreated with vitamin E was significantly lower than that in the control group and hydrogen-peroxide-treated group, especially in those pretreated with 100 µmol/L vitamin E. The differentially expressed genes (DEGs) concerning cell death involved in apoptosis (RIPK1, TLR7, CASP8, and CASP8AP2), pyroptosis (NLRP3, IL-1ß, and IRAK2), and ferroptosis (TFRC and PTGS2). The abundances of IL-1ß, IRAK2, NLRP3, CASP8, CASP8AP2, RIPK1, and TLR7 were significantly increased in the C1 group and decreased in T1 group, while TFRC and PTGS2 were increased in T1 group. (4) Conclusions: oxidative stress induced by hydrogen peroxide caused cellular damage and death in sheep hepatocytes. Pretreatment with vitamin E effectively reduced intracellular ROS levels and protected the hepatocytes from cell death by regulating gene expression associated with apoptosis (RIPK1, TLR7, CASP8, and CASP8AP2) and pyroptosis (NLRP3, IL-1ß, and IRAK2), but not ferroptosis (TFRC and PTGS2).


Assuntos
Antioxidantes/farmacologia , Ferroptose/genética , Expressão Gênica/efeitos dos fármacos , Hepatócitos/metabolismo , Peróxido de Hidrogênio/farmacologia , Estresse Oxidativo/efeitos dos fármacos , Piroptose/genética , Vitamina E/farmacologia , Animais , Sobrevivência Celular/efeitos dos fármacos , Células Cultivadas , Ferroptose/efeitos dos fármacos , Regulação da Expressão Gênica , Hepatócitos/efeitos dos fármacos , Fígado/citologia , Piroptose/efeitos dos fármacos , RNA-Seq/métodos , Espécies Reativas de Oxigênio/metabolismo , Ovinos , Transdução de Sinais/efeitos dos fármacos
5.
Cell Death Dis ; 12(7): 706, 2021 07 15.
Artigo em Inglês | MEDLINE | ID: mdl-34267193

RESUMO

Ferroptosis, a newly defined mode of regulated cell death caused by unbalanced lipid redox metabolism, is implicated in various tissue injuries and tumorigenesis. However, the role of ferroptosis in stem cells has not yet been investigated. Glutathione peroxidase 4 (GPX4) is a critical suppressor of lipid peroxidation and ferroptosis. Here, we study the function of GPX4 and ferroptosis in hematopoietic stem and progenitor cells (HSPCs) in mice with Gpx4 deficiency in the hematopoietic system. We find that Gpx4 deletion solely in the hematopoietic system has no significant effect on the number and function of HSPCs in mice. Notably, hematopoietic stem cells (HSCs) and hematopoietic progenitor cells lacking Gpx4 accumulated lipid peroxidation and underwent ferroptosis in vitro. α-Tocopherol, the main component of vitamin E, was shown to rescue the Gpx4-deficient HSPCs from ferroptosis in vitro. When Gpx4 knockout mice were fed a vitamin E-depleted diet, a reduced number of HSPCs and impaired function of HSCs were found. Furthermore, increased levels of lipid peroxidation and cell death indicated that HSPCs undergo ferroptosis. Collectively, we demonstrate that GPX4 and vitamin E cooperatively maintain lipid redox balance and prevent ferroptosis in HSPCs.


Assuntos
Antioxidantes/farmacologia , Ferroptose/efeitos dos fármacos , Células-Tronco Hematopoéticas/efeitos dos fármacos , Peroxidação de Lipídeos/efeitos dos fármacos , Fosfolipídeo Hidroperóxido Glutationa Peroxidase/metabolismo , Deficiência de Vitamina E/tratamento farmacológico , Vitamina E/farmacologia , Animais , Células Cultivadas , Modelos Animais de Doenças , Feminino , Transplante de Células-Tronco Hematopoéticas , Células-Tronco Hematopoéticas/enzimologia , Células-Tronco Hematopoéticas/patologia , Masculino , Camundongos Endogâmicos C57BL , Camundongos Knockout , Fosfolipídeo Hidroperóxido Glutationa Peroxidase/genética , Deficiência de Vitamina E/enzimologia , Deficiência de Vitamina E/genética , Deficiência de Vitamina E/patologia
6.
Andrologia ; 53(10): e14185, 2021 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-34275146

RESUMO

The role of quercetin and vitamin E treatment against streptozotocin (STZ)-induced testicular abnormalities in diabetic rats and the possible mechanism of action they use for protection were investigated. Diabetes was induced by STZ (45 mg/kg i.p. once) and blood glucose was determined. Plasmatic insulin, testosterone, luteinising hormone and follicle-stimulating hormone (FSH) were determined by ELISA. Levels of cytochrome c, caspase 3 and caspase 9 were evaluated by immunohistochemistry, while lesions were viewed by histology. Insulin played a role in testicular protection against male infertility through modulation of luteinising hormone (LH). This consequently increased Leydig and Sertoli cells and maturation of germ cells with the attached epididymis having abundant spermatozoa. The study showed a positive correlation in the levels of LH, FSH and testosterone; it was further established that all treatments normalised diabetes-induced alterations. Treatment with quercetin and vitamin E resulted in 34% decrease of apoptogenic cytochrome c release. This protected the testes against excessive apoptosis by decreasing caspase 3 and caspase 9 activation by up to 30 and 28% respectively (p < .05). Histology also showed that treatment prevented testicular cell death. The findings show that quercetin/vitamin E possess free radical scavenging properties that protected against testicular damage in diabetes. This suggests the possibility of pharmaco-therapeutic intervention.


Assuntos
Diabetes Mellitus Experimental , Quercetina , Animais , Apoptose , Diabetes Mellitus Experimental/tratamento farmacológico , Masculino , Estresse Oxidativo , Quercetina/farmacologia , Ratos , Ratos Wistar , Testículo , Testosterona , Vitamina E/farmacologia
7.
Nutrients ; 13(6)2021 Jun 07.
Artigo em Inglês | MEDLINE | ID: mdl-34200192

RESUMO

Vitamin E was identified as a lipophilic compound essential to maintain rat pregnancy. Low vitamin E intake during early pregnancy associates with congenital malformations and embryonic loss in animals and with miscarriage and intrauterine growth restriction in humans. Vitamin E protects cell membranes from lipoperoxidation and exerts non-antioxidant activities. Its function can be restored by vitamin C; thus, intake and circulating levels of both micronutrients are frequently analyzed together. Although substantial vitamin E inadequacy was reported worldwide, its consumption in Latin America (LatAm) is mostly unknown. Using data from the Latin American Study of Nutrition and Health (Estudio Latinoamericano de Nutrición y Salud, ELANS), we evaluated vitamin E and C intake in women of reproductive age (WRA) from eight LatAm countries and identified their main food sources. Two non-consecutive 24-h dietary recalls in 3704 women aged from 15 to 49 years and living in urban locations showed low average intake of vitamin E (7.9 mg/day vs. estimated average requirement (EAR) of 12 mg/day) and adequate overall vitamin C consumption (95.5 mg/day vs. EAR of 60 mg/day). The mean regional inadequacy was 89.6% for vitamin E and 36.3% for vitamin C. The primary food sources of vitamin E were fats and oils, as well as vegetables. Vitamin C intake was explained mainly by the consumption of fruit juices, fruits, and vegetables. Combined deficient intake of both vitamins was observed in 33.7% of LatAm women. Although the implications of low antioxidant vitamins' consumption in WRA are still unclear, the combined deficient intake of both vitamins observed in one-third of ELANS participants underscores the need for further research on this topic.


Assuntos
Ácido Ascórbico/farmacologia , Saúde , Estado Nutricional , Reprodução , Vitamina E/farmacologia , Adolescente , Adulto , Fatores Etários , Comportamento Alimentar , Feminino , Alimentos , Humanos , América Latina , Pessoa de Meia-Idade , Adulto Jovem
8.
J Nutr Biochem ; 96: 108806, 2021 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-34147603

RESUMO

Many cancer patients receive their classical therapies together with vitamin supplements. However, the effectiveness of these strategies is on debate. Here we aimed to evaluate how vitamin E supplementation affects the anticancer effects of interferon (IFN-α) using an early-model of liver cancer development (initiation-promotion, IP). Male Wistar rats subjected to this model were divided as follows: untreated (IP), IP treated with recombinant IFN-α-2b (6.5  ×  105 U/kg), IP treated with vitamin E (50 mg/kg), and IP treated with combination of vitamin E and IFN-α-2b. After treatments rats were fasted and euthanized and plasma and livers were collected. Combined administration of vitamin E and IFN-α-2b induced body weight drop, increased liver apoptosis, and low levels of hepatic lipids. Interestingly, vitamin E and IFN-α-2b combination also induced an increase in altered hepatic foci number, but not in size. It seems that vitamin E acts on its antioxidant capability in order to block the oxidative stress induced by IFN-α-2b, blocking in turn its beneficial effects on preneoplastic livers, leading to harmful final effects. In conclusion, this study shows that vitamin E supplementation in IFN-α-2b-treated rats exerts unwanted effects; and highlights that in spite of being natural, nutritional supplements may not always exert beneficial outcomes when used as complementary therapy for the treatment of cancer.


Assuntos
Anticarcinógenos/farmacologia , Interferon alfa-2/farmacologia , Neoplasias Hepáticas/prevenção & controle , Vitamina E/farmacologia , Vitaminas/farmacologia , Animais , Carcinogênese/efeitos dos fármacos , Carcinogênese/patologia , Interações Medicamentosas , Fígado/efeitos dos fármacos , Fígado/patologia , Neoplasias Hepáticas/patologia , Masculino , Ratos Wistar
9.
Andrologia ; 53(8): e14140, 2021 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-34152619

RESUMO

Valproic acid (VPA) is a teratogenic antiepileptic, causing alterations in oxidative stress in prenatal development, being altered the development of the male reproductive system. The purpose of this study was to determine the protective effect of vitamin E (VE) on the testicular development in embryos, foetuses and pubertal mice exposed to VPA, VPA+VE and only VE. Sixty pregnant adult female mice were used, to which they were administered 600 mg/kg of VPA (VPA groups), 600 mg/kg of VPA and 200 IU of VE (VPA+VE groups), 200 IU VE (VE groups) and 0.3 ml of 0.9% physiological solution (control groups), showing at 12.5 days post-coital (dpc), 17.5 dpc and 6 weeks postnatal testicular development, and proliferative and apoptotic indices. The groups treated with VPA presented a smaller testicular volume, with greater interstitial space and a delay in the conformation of the testicular cords, shorter lengths and diameters of the germinal epithelium, a smaller number of germline and somatic cells, an increase in cells apoptotic and less proliferation, with significant differences. VE-treated groups behaved similarly to controls. In conclusion, VE reduces the effects caused by VPA throughout testicular development, from embryonic stages, continuing until pubertal stages.


Assuntos
Ácido Valproico , Vitamina E , Animais , Anticonvulsivantes/toxicidade , Feminino , Masculino , Camundongos , Estresse Oxidativo , Gravidez , Testículo , Ácido Valproico/toxicidade , Vitamina E/farmacologia
10.
Am J Physiol Regul Integr Comp Physiol ; 321(1): R49-R61, 2021 07 01.
Artigo em Inglês | MEDLINE | ID: mdl-34075811

RESUMO

Posttraumatic stress disorder (PTSD) has been associated with an increase in risk of cardiovascular disease (CVD). The goal of this study was to determine if peripheral vascular dysfunction, a precursor to CVD, was present in young adults with PTSD, and if an acute antioxidant (AO) supplementation could modify this potential PTSD-induced vascular dysfunction. Thirteen individuals with PTSD were recruited for this investigation and were compared with 35 age- and sex-matched controls (CTRL). The PTSD group participated in two visits, consuming either a placebo (PTSD-PL) or antioxidants (PTSD-AO; vitamins C and E; α-lipoic acid) before their visits, whereas the CTRL subjects only participated in one visit. Upper and lower limb vascular functions were assessed via flow-mediated dilation and passive leg movement technique. Heart rate variability was utilized to assess autonomic nervous system modulation. The PTSD-PL condition, when compared with the CTRL group, reported lower arm and leg microvascular function as well as sympathetic nervous system (SNS) predominance. After acute AO supplementation, arm, but not leg, microvascular function was improved and SNS predominance was lowered to which the prior difference between PTSD group and CTRL was no longer significant. Young individuals with PTSD demonstrated lower arm and leg microvascular function as well as greater SNS predominance when compared with age- and sex-matched controls. Furthermore, this lower vascular/autonomic function was augmented by an acute AO supplementation to the level of the healthy controls, potentially implicating oxidative stress as a contributor to this blunted vascular/autonomic function.


Assuntos
Ácido Ascórbico/farmacologia , Sistema Nervoso Autônomo/efeitos dos fármacos , Transtornos de Estresse Pós-Traumáticos/tratamento farmacológico , Ácido Tióctico/farmacologia , Vitamina E/farmacologia , Adulto , Antioxidantes/administração & dosagem , Antioxidantes/farmacologia , Ácido Ascórbico/administração & dosagem , Pressão Sanguínea , Estudos de Casos e Controles , Quimioterapia Combinada , Feminino , Humanos , Masculino , Ácido Tióctico/administração & dosagem , Vitamina E/administração & dosagem , Adulto Jovem
11.
Colloids Surf B Biointerfaces ; 205: 111914, 2021 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-34130211

RESUMO

Currently, multidrug resistance (MDR) is one of the major reasons for failure in clinical cancer chemotherapy. Overexpression of the ATP binding cassette (ABC) transporter P-glycoprotein (P-gp), which significantly increases the efflux of anticancer drugs from tumor cells, enhances MDR. In the past few decades, four generations of P-gp inhibitors have appeared. However, they are limited in clinical application due to their severe toxic side effects. As a P-gp inhibitor and carrier for loading chemotherapy agents, TPGS has received increasing attention due to its advantages and unique properties of reversing MDR. TPGS is an amphipathic agent that increases the solubility of most chemotherapy drugs and decreases severe side effects. In addition, TPGS is an excellent carrier with P-gp-inhibiting ability. In this review, we summarize the latest articles on TPGS-based nanodelivery systems to prevent MDR.


Assuntos
Antineoplásicos , alfa-Tocoferol , Membro 1 da Subfamília B de Cassetes de Ligação de ATP , Antineoplásicos/farmacologia , Resistência a Múltiplos Medicamentos , Resistencia a Medicamentos Antineoplásicos , Polietilenoglicóis/farmacologia , Succinatos/farmacologia , Vitamina E/farmacologia , alfa-Tocoferol/farmacologia
12.
Theriogenology ; 170: 91-106, 2021 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-34000522

RESUMO

Dairy cows are susceptible to reproductive disorders, which are thought to be associated with oxidative stress. In the study, we investigated the effects of vitamin E (VE) and selenium (Se) on the proliferation, apoptosis, and steroidogenesis in bovine ovarian granulosa cells under hydrogen peroxide (H2O2) - induced oxidative stress and elaborated the underlying mechanisms. Our results showed that VE or Se could stimulate the granulosa cell proliferation, possibly due to up-regulating the expression of CCND1 and decreasing the P21 levels under oxidative stress. VE or Se treatment also increased the secretion of estradiol (E2) and progesterone (P4), which could be owing to improving the expression of genes associated with steroidogenesis (StAR, HSD3ß1, and CYP19A1) expression. VE or Se treatment down-regulated the apoptosis-related genes (BAX, CASP3) expression and decreased cell apoptosis. Furthermore, VE or Se treatment inhibited reactive oxidative species (ROS) and malondialdehyde (MDA) generation, increased total antioxidant capacity (T-AOC), and the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px). Additionally, VE or Se treatment also alleviated the endoplasmic reticulum stress, activated the nuclear factor erythroid 2-related factor 2 (NRF2), and up-regulated the expression of its downstream genes, including NQO1, HO-1, GCLM, GCLC. More importantly, compared with either VE or Se treatment alone, their combined treatment showed a better protective effect against oxidative damage. Overall, our results indicated that VE and Se synergistically stimulated the granulosa cell proliferation and steroidogenesis, decreased cell apoptosis, mitigated the endoplasmic reticulum stress by activating the NRF2 signal pathway.


Assuntos
Selênio , Animais , Antioxidantes/metabolismo , Apoptose , Bovinos , Suplementos Nutricionais , Feminino , Células da Granulosa/metabolismo , Peróxido de Hidrogênio/metabolismo , Fator 2 Relacionado a NF-E2 , Estresse Oxidativo , Selênio/farmacologia , Vitamina E/farmacologia
13.
Trop Anim Health Prod ; 53(2): 330, 2021 May 17.
Artigo em Inglês | MEDLINE | ID: mdl-34002255

RESUMO

The sperm membrane is damaged in cryopreservation processes; this damage can be minimized using antioxidants such as vitamin E. The objective of the present study was to evaluate the effect of the addition of vitamin "E" on the viability of ram sperm during preservation processes. Two experiments were carried out; in the first, 32 ejaculates were used, which after evaluation were divided into two aliquots for processing; the first received Triladyl + vitamin "E" (T + E), and the second received only Triladyl (T); these aliquots were cooled and stored at 5 °C for 24 h. The viability (sperm motility, integrity, and membrane permeability) was evaluated at 0 and 24 h after dilution. In the second experiment, the same procedure was performed as experiment 1, except that the samples were also frozen, and the viability was evaluated at zero and 48 h post-freezing. Dependent variables were analyzed using mixed models in a split plot design. In experiment 1, the integrity and permeability of the sperm membrane was better in the group: "T + E" (P <0.05). In experiment 2, the vitamin significantly improved (P <0.05) the sperm viability. It is concluded that the addition of vitamin "E" improves sperm viability.


Assuntos
Preservação do Sêmen , Animais , Criopreservação/veterinária , Crioprotetores , Masculino , Preservação do Sêmen/veterinária , Ovinos , Motilidade Espermática , Espermatozoides , Vitamina E/farmacologia , Vitaminas
14.
J Vet Sci ; 22(3): e33, 2021 May.
Artigo em Inglês | MEDLINE | ID: mdl-33908207

RESUMO

Very virulent infectious bursal disease virus (vvIBDV) causes high mortality in chickens but measures to reduce the mortality have not been explored. Chickens (8-9 weeks) were treated with 3 agents before and during vvIBDV inoculation. Dexamethasone treatment reduced the mortality of infected chickens (40.7% vs. 3.7%; p < 0.001), but treatment with aspirin or vitamin E plus selenium did not affect the mortality. The bursa of Fabricius appeared to have shrunk in both dead and surviving chickens (p < 0.01). The results indicate that dexamethasone can reduce mortality in vvIBDV-infected chickens and may provide therapeutic clues for saving individual birds infected by the virus.


Assuntos
Infecções por Birnaviridae/veterinária , Galinhas , Dexametasona/farmacologia , Imunossupressores/farmacologia , Doenças das Aves Domésticas/prevenção & controle , Animais , Anti-Inflamatórios , Anti-Inflamatórios não Esteroides/administração & dosagem , Anti-Inflamatórios não Esteroides/farmacologia , Antioxidantes/administração & dosagem , Antioxidantes/farmacologia , Aspirina/administração & dosagem , Aspirina/farmacologia , Infecções por Birnaviridae/mortalidade , Infecções por Birnaviridae/prevenção & controle , Imunossupressores/administração & dosagem , Vírus da Doença Infecciosa da Bursa/fisiologia , Doenças das Aves Domésticas/mortalidade , Selênio/administração & dosagem , Selênio/farmacologia , Vitamina E/administração & dosagem , Vitamina E/farmacologia , Vitaminas/administração & dosagem , Vitaminas/farmacologia
15.
J Biol Regul Homeost Agents ; 35(2): 457-471, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33823569

RESUMO

Diet pattern is an emerging risk factor for renal disease. The mechanism by which high-fat high fructose (western) diet mediates renal injury is not yet fully understood. The objective of the present study was to investigate the relationship between endoplasmic reticulum (ER) stress and autophagy in the development of renal impairment and aggravation of the inflammatory response. Eighty male rats were randomly divided into four groups as follows: a standard diet-fed (ConD), a high-fat high fructose diet fed (HFHF-V), ConD fed and orally supplemented with vitamin E (ConD-E), and HFHF fed and orally supplemented vitamin E (HFHF-E). After 12 weeks, either lipopolysaccharide (LPS) or saline was injected. We found that upregulation of endoplasmic reticulum stress-related proteins rendered the cells susceptible to injury induced by dysbiosis and microbiota-derived metabolites. A downregulation of autophagy and upregulation of caspase-12 resulted in the loss of intestinal integrity and renal tubular injury. Maintained ER stress also increased the inflammatory response to LPS. In contrast, vitamin E effectively ameliorated ER stress and promoted autophagy to protect intestinal and renal tissues. Our results provide insight into the influences of sustained ER stress activation and autophagy inhibition on the development of renal injury, which may contribute also to the enhanced inflammatory response.


Assuntos
Estresse do Retículo Endoplasmático , Lipopolissacarídeos , Animais , Apoptose , Autofagia , Dieta Ocidental , Disbiose , Lipopolissacarídeos/toxicidade , Masculino , Ratos , Vitamina E/farmacologia
16.
Environ Toxicol ; 36(7): 1375-1388, 2021 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-33818898

RESUMO

Fusarium mycotoxins are one of the largest families of mycotoxins. Among these mycotoxins, deoxynivalenol is the most widespread pollutant of grains. However, the mechanism underlying the effect of deoxynivalenol on cytotoxicity in human brain endothelial cells was still unclear. This study examined whether deoxynivalenol induced oxidative stress-associated cytotoxicity in primary human brain endothelial cells (HBEC-5i), and explored whether Vitamin E (VE), a selective antioxidant, had protective effects on deoxynivalenol-treated cells. Deoxynivalenol (10-50 µM) concentration-dependently induced cytotoxicity in HBEC-5i cells. Deoxynivalenol (IC50 = 20 µM) activated mitochondrial apoptotic pathway by modulating antioxidant protein expressions (Nrf2, HO-1 and NQO1). More significantly, pre-treatment with VE (20 µM) attenuated the deoxynivalenol-induced cytotoxicity in this cell model. Together, VE significantly alleviated the apoptotic effects of deoxynivalenol in HBEC-5i cells suggesting that it protected the cells against deoxynivalenol-induced oxidative damage. Our findings provided new insight that VE had the potential to ameliorate neurotoxicity of deoxynivalenol.


Assuntos
Micotoxinas , Vitamina E , Encéfalo/metabolismo , Células Endoteliais/metabolismo , Humanos , Micotoxinas/toxicidade , Fator 2 Relacionado a NF-E2/metabolismo , Estresse Oxidativo , Espécies Reativas de Oxigênio , Tricotecenos , Vitamina E/farmacologia
17.
Andrologia ; 53(7): e14075, 2021 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-33877689

RESUMO

Hyperthermia (HT) is a significant risk factor for male infertility. Most researchers investigated the effect of localized and short-term HT on male fertility. This study aimed to assess the harmful impacts of prolonged and generalized HT on testicular histology and ultrastructure in rats. The possible protective effects of vitamin E (Vit E), Vit C, and their combination were also investigated. Thirty male adult Wister rats were used (5 groups). 1- control, 2- HT, 3- Vit C, 4- Vit E, and 5- Vit C + Vit E. Rats in groups 2-5 were subjected to HT (41°C), 1 hr daily for 2 weeks. HT-induced a significant decrease in body weight gain, food and water intake, and serum testosterone. HT showed a damaging effect on the testicular and coda epididymis tissue. HT significantly (p ≤ .05) produced oxidative stress (decreased serum catalase (145.49 ± 8.98), glutathione peroxidase (20.27 ± 4.46), superoxide dismutase (2.68 ± 0.54), and reduced glutathione (5.18 ± 0.33), and increased malondialdehyde (9.46 ± 1.55). Vit E alone and combined with Vit C, significantly protected the gonads against the deleterious effects of HT. The results recommended that prolonged HT of the whole body is harmful to male fertility. Prophylactic therapy with Vit E could help decrease the HT-induced male gonadal harm.


Assuntos
Antioxidantes , Ácido Ascórbico , Animais , Antioxidantes/farmacologia , Ácido Ascórbico/farmacologia , Hipertermia , Masculino , Estresse Oxidativo , Ratos , Superóxido Dismutase/metabolismo , Testículo/metabolismo , Vitamina E/farmacologia
18.
Trop Anim Health Prod ; 53(2): 298, 2021 Apr 30.
Artigo em Inglês | MEDLINE | ID: mdl-33928444

RESUMO

The objective of this study was to determine the effects of supplemental Bacillus subtilis (BS, 0.5 × 1011 CFU/day), injectable vitamin E and selenium (ES, 1000 mg α-tocopherol acetate and 10 mg sodium selenite), or both during the transition period on health parameters and the incidence of retained fetal membranes (RFM) of dairy cows under tropical conditions (average temperature humidity index = 77.0). Thirty-two crossbred Holstein-Friesian cows were used in a randomized design trial with a 2 × 2 factorial arrangement of treatments. Cows were randomly assigned to one of four treatments, including no supplementation (CON), single intramuscular injection of ES on day - 21 before the expected calving date (ES), daily oral supplementation of BS between day - 21 and day 21 relative to calving, or both ES and BS. Body condition score (BCS) and blood samples were collected on days - 28, - 14, 0, 14, and 28 relative to calving. Mean concentrations of corpuscular hemoglobin were higher (33.12 vs 34.03 g/dL, p = 0.06) and platelets were lower (380.97 vs 302.32 × 103/µL, p = 0.10) with ES than without ES. Cows fed supplemental BS had lower concentrations of creatinine and albumin and tended to have lower AST and ß-hydroxybutyrate (BHBA) levels. However, concentrations of glucose were higher for cows fed BS than for those without BS. No differences in the incidence of RFM were observed. In summary, supplemental B. subtilis could reduce indicators of negative energy balance by increasing glucose and lowering BHBA and improve health parameters by keeping WBCs and monocytes in a healthy range during the transition period.


Assuntos
Lactação , Selênio , Ácido 3-Hidroxibutírico , Animais , Bacillus subtilis , Bovinos , Dieta/veterinária , Suplementos Nutricionais , Feminino , Leite , Período Pós-Parto , Selênio/farmacologia , Vitamina E/farmacologia
19.
Artigo em Inglês | MEDLINE | ID: mdl-33820770

RESUMO

Today, antivirulence compounds that attenuate bacterial pathogenicity and have no interference with bacterial viability or growth are introduced as the next generation of antibacterial agents. However, the development of such compounds that can be used by humans is restricted by various factors, including the need for extensive economic investments, the inability of many molecules to penetrate the membrane of Gram-negative bacteria, and unfavorable pharmacological properties and cytotoxicity. Here, we take a new and different look into two frequent supplements, vitamin E and K1, as anti-quorum-sensing agents against Pseudomonas aeruginosa, a pathogen that is hazardous to human life and responsible for several diseases. Both vitamins showed significant anti-biofilm activity (62% and 40.3% reduction by vitamin E and K1, respectively), and the expression of virulence factors, including pyocyanin, pyoverdine, and protease, was significantly inhibited, especially in the presence of vitamin E. Cotreatment of constructed biofilms with these vitamins plus tobramycin significantly reduced the number of bacterial cells sheltered inside the impermeable matrix (71.6% and 69% by a combination of tobramycin and vitamin E or K1, respectively). The in silico studies, besides the similarities of chemical structures, reinforce the possibility that both vitamins act through inhibition of the PqsR protein. This is the first report of the antivirulence and antipathogenic activity of vitamin E and K1 against P. aeruginosa and confirms their potential for further research against other multidrug-resistant bacteria.


Assuntos
Pseudomonas aeruginosa , Vitamina E , Antibacterianos/farmacologia , Proteínas de Bactérias/genética , Biofilmes , Humanos , Percepção de Quorum , Fatores de Virulência , Vitamina E/farmacologia , Vitaminas/farmacologia
20.
J Dairy Sci ; 104(6): 7154-7167, 2021 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-33773776

RESUMO

Diseases that occur during the transition period are exacerbated when cows are unable to cope with an increased pro-oxidant load that results in oxidative stress. Dairy cattle are routinely supplemented with the vitamin E analog α-tocopherol to mitigate the severity of oxidative stress. Nonetheless, oxidative stress remains a disease predisposing condition for many dairy cattle. A better method of optimizing the antioxidant functions of vitamin E is needed. α-Tocopherol is only 1 of 8 analogs of vitamin E, all of which have varying antioxidant properties in other mammals, albeit a shorter physiological half-life compared with α-tocopherol. A primary bovine mammary endothelial cell oxidant challenge model was used to determine functions of certain vitamin E analogs. The aim of this study was to determine if other analogs, namely γ-tocopherol or γ-tocotrienol, have antioxidative functions in bovine cells and if these functions may protect cellular viability and endothelial function from oxidant damage. Physiological (10 µM) and supraphysiological (50 µM) concentrations of γ-tocopherol and γ-tocotrienol had a greater capacity to reduce accumulated reactive oxygen species derived from a nitric oxide donating pro-oxidant antagonist, when compared with α-tocopherol, after 30 min to 6 h of treatment. Further, γ-tocotrienol (10 µM) decreased cell cytotoxicity to a greater amount than other analogs at like concentrations, whereas γ-tocopherol (10 µM) reduced lipid peroxidation and apoptosis more effectively than other analogs. Last, α-tocopherol (5 and 10 µM) and γ-tocopherol (5 and 10 µM) significantly slowed pro-oxidant induced loss of endothelial cell barrier integrity over a 48-h period using an electrical cell-substrate impedance sensing system. Concerningly, γ-tocotrienol drastically reduced the endothelial barrier integrity at only 5 µM despite no apparent effect on cellular viability at like concentrations. γ-Tocotrienol, however, was also the only analog to show significant cytotoxicity and reductions in viability at supraphysiological doses (25 and 50 µM). Our results suggest that γ-tocopherol has antioxidant activities that reduces cellular damage and loss of function due to oxidant challenge as effectively as α-tocopherol. These data set the foundation for further investigation into the antioxidant properties of vitamin E analogs in other bovine cells types or whole animal models.


Assuntos
Células Endoteliais , Oxidantes , Animais , Antioxidantes , Bovinos , Vitamina E/farmacologia , alfa-Tocoferol/farmacologia
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