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A novel Artemisinin/Quercetin/Zinc (Art/Q/Zn) mixed ligand complex was synthesized, tested for its antiviral activity against coronavirus (SARS-CoV-2), and investigated for its effect against toxicity and oxidative stress induced by acrylamide (Acy), which develops upon cooking starchy foods at high temperatures. The synthesized complex was chemically characterized by performing elemental analysis, conductance measurements, FT-IR, UV, magnetic measurements, and XRD. The morphological surface of the complex Art/Q/Zn was investigated using scanning and transmission electron microscopy (SEM and TEM) and energy dispersive X-ray analysis (XRD). The in vitro antiviral activity of the complex Art/Q/Zn against SARS-CoV-2 and its in vivo activity against Acy-induced toxicity in hepatic and pulmonary tissues were analyzed. An experimental model was used to evaluate the beneficial effects of the novel Art/Q/Zn novel complex on lung and liver toxicities of Acy. Forty male rats were randomly divided into four groups: control, Acy (500 mg/Kg), Art/Q/Zn (30 mg/kg), and a combination of Acy and Art/Q/Zn. The complex was orally administered for 30 days. Hepatic function and inflammation marker (CRP), tumor necrosis factor, interleukin-6 (IL-6), antioxidant enzyme (CAT, SOD, and GPx), marker of oxidative stress (MDA), and blood pressure levels were investigated. Histological and ultrastructure alterations and caspase-3 variations (immunological marker) were also investigated. FT-IR spectra revealed that Zn (II) is able to chelate through C=O and C-OH (Ring II) which are the carbonyl oxygen atoms of the quercetin ligand and carbonyl oxygen atom C=O of the Art ligand, forming Art/Q/Zn complex with the chemical formula [Zn(Q)(Art)(Cl)(H2O)2]â 3H2O. The novel complex exhibited a potent anti-SARS-CoV-2 activity even at a low concentration (IC50 = 10.14 µg/ml) and was not cytotoxic to the cellular host (CC50 = 208.5 µg/ml). Art/Q/Zn may inhibit the viral replication and binding to the angiotensin-converting enzyme-2 (ACE2) receptor and the main protease inhibitor (MPro), thereby inhibiting the activity of SARS-CoV-2 and this proved by the molecular dynamics simulation. It alleviated Acy hepatic and pulmonary toxicity by improving all biochemical markers. Therefore, it can be concluded that the novel formula Art/Q/Zn complex is an effective antioxidant agent against the oxidative stress series, and it has high inhibitory effect against SARS-CoV-2.
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Artemisininas , COVID-19 , Masculino , Animais , Ratos , Antioxidantes/farmacologia , Quercetina/farmacologia , SARS-CoV-2 , Zinco/farmacologia , Ligantes , Espectroscopia de Infravermelho com Transformada de Fourier , Artemisininas/farmacologia , Antivirais/farmacologia , Acrilamida/toxicidade , OxigênioRESUMO
Background: Prevalence of obesity is increasing worldwide. Obesity is associated with incidences of metabolic disorders and cardiovascular diseases and the risk of having it rose sharply during the COVID-19 pandemic. Obesity is associated with oxidative stress, inflammatory markers and hepatic disorders and has become one of the silent killer diseases affecting global health. Methods: This study examined the effects of obesity on liver functions (ALT, AST and LDH), lipid profile (TG, TC, HDL-c, LDL-c and vLDL-c), tumour necrosis factor alpha (TNF-α), inflammatory marker, C-reactive protein (CRP), leptin hormone and antioxidant enzymes (CAT, SOD and GPx) and lipid peroxidation marker (MDA) in liver homogenates besides histological structure of the liver tissues and assessment of DNA damage. Fifty male Wistar rats were used and they were divided into five treatment groups: I-Control group, II-high-fat diet (HFD) treated group (Obesity) group, III-HFD plus Orlistat (ORL), IV-HFD plus metformin (Met) and V- HFD plus ORL plus Met. Results: Experimentally-induced obesity caused a significant increase in liver enzymes including lipid markers (triglycerides and total cholesterol), inflammatory markers, tumour markers and lipid peroxidation markers and a concurrent decline in antioxidant enzymes and damage of liver main structures characterised by presence of congestion and accumulation of mononuclear inflammatory cells in blood sinusoids. In contrast, groups treated with either ORL or Met or both group, we recorded restoration of normal hepatic structures and a decline in DNA damage, liver enzymes and antioxidant levels. The best restoration and amelioration were observed in the group treated with a combination of ORL and Met. Conclusion: Our findings indicated the synergistic effect of ORL and Met in ameliorating hepatic functions and lipid profile, alleviating inflammation, genotoxicity and side effects of experimentally-induced obesity.
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Exposure to cadmium chloride (CdCl2) causes an imbalance in the oxidant status of the body by triggering the release of reactive oxygen species (ROS). This study investigated the effect of Rosa damascena (R. damascena) extract on oxidative stress, hepatotoxicity, and the injured cardiac tissue of male rats exposed to CdCl2. Forty male Wistar albino rats were divided into four groups: the vehicle control (1 mg/kg normal saline), the CdCl2-treated group (5 mg/kg), the R. damascena extract group (100 mg Kg), and the combination of CdCl2 and R. damascena extract group. Male rats exposed to CdCl2 showed multiple significant histopathological changes in the liver and heart, including inflammatory cell infiltration and degenerative alterations. Successive exposure to CdCl2 elevated the levels of hepatic and cardiac reactive oxygen species (ROS), malondialdehyde (MDA), tumour necrosis factor-alpha) (TNF-α) and interleukin -6 (IL-6) and decreased antioxidant defences. The extracts significantly increased the levels of glutathione, superoxide dismutase (SOD), and catalase (CAT), whereas it dramatically decreased the levels of lipid peroxidation (LPO), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and the mRNA of TNF-α and IL-6. R. damascena administration prevented liver and heart injury; suppressed excessive ROS generation, LPO, and inflammatory responses; and enhanced antioxidant defences. In addition, R. damascena upregulated the mRNA of TNF-α and IL-6 in CdCl2-administered male rats. In conclusion, R. damascena modulated the oxidative stress and inflammation induced by CdCl2. The hepatic and cardiac tissue damage and histopathological alterations resulting from the CdCl2-induced oxidative stress were counteracted by the administration of R. damascena extracts. R. damascena enhanced antioxidant defence enzymes in male rats.
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In this study, metal cefotaxime complexes of Ca(II), Cr(III), Cu(II), Zn(II), and Se(VI) were synthesized and characterized by elemental analysis, conductance measurements, IR, electronic spectra, magnetic measurements, 1HNMR, and XRD, as well as by scanning electron microscopy (SEM) and transmission electron microscopy (TEM). The lower values for molar conductance refer to the nonelectrolyte nature of the complexes. The FTIR and 1H-NMR spectra for the metal complexes of cefotaxime proved that the free cefotaxime antibiotic ligand acted as a monoanionic tridentate ligand through the oxygen atoms of lactam carbonyl, the carboxylate group, and the nitrogen atoms of the amino group. From the magnetic measurements and electronic spectral data, octahedral structures were proposed for the Cr(III) and Se(VI) complexes, while the Cu(II) complex had tetragonal geometry. This study aimed to investigate the effects of cefotaxime and cefotaxime metal complexes on oxidative stress using antioxidant assays including DPPH, ORAC, FARAB, and ABTS, a metal chelation assay, as well as the inhibition of the viability of cancer cells (HepG-2). Regarding the antibacterial activity, the cefotaxime metal complexes were highly effective against both Bacillus subtilis and Escherichia coli. In conclusion, the cefotaxime metal complexes exhibited highly antioxidant activities. The cefotaxime metal complexes with Zn and Se inhibited HepG-2 cellular viability. Thus, the cefotaxime metal complexes elicited promising results as potent antioxidant and anticancer agents against HepG-2, with potent antibacterial activities at a much lower concentration.
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The present study aimed to investigate the effect of the royal jelly (RJ) on hepatotoxicity induced by molybdenum nanoparticles (MoO3-NPs), cadmium chloride (CdCl2), or their combination in male rats at biochemical, inflammation, immune response, histological, and ultrastructural levels. The physicochemical properties of MoO3-NPs have been characterized, as well as their ultrastructural organization. A rat experimental model was employed to assess the liver toxicity of MoO3-NPs, even in combination with CdCl2. Different cellular studies indicate divergent mechanisms, from increased reactive oxygen species production to antioxidative damage and cytoprotective activity. Seventy male rats were allocated to groups: (i) control; (ii) MoO3-NPs (500 mg/kg); (iii) CdCl2 (6.5 mg/kg); (iv) RJ (85 mg/kg diluted in saline); (v) MoO3-NPs followed by RJ (30 min after the MoO3-NPs dose); (vi) CdCl2 followed by RJ; and (vii) a combination of MoO3-NPs and CdCl2, followed by RJ, for a total of 30 successive days. Hepatic functions, lipid profile, inflammation marker (CRP), antioxidant biomarkers (SOD, CAT, GPx, and MDA), and genotoxicity were examined. Histological changes, an immunological marker for caspase-3, and transmission electron microscope variations in the liver were also investigated to indicate liver status. The results showed that RJ alleviated the hepatotoxicity of MoO3-NPs and/or CdCl2 by improving all hepatic vitality markers. In conclusion, the RJ was more potent and effective as an antioxidant over the oxidative damage induced by the combination of MoO3-NPs and CdCl2.
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Medicinal uses and applications of metals and their complexes are of increasing clinical and commercial importance. The ligation behavior of quercetin (Q), which is a flavonoid, and its Zn (II) (Q/Zn) complex were studied and characterized based on elemental analysis, molar conductance, Fourier-transform infrared (FTIR) spectra, electronic spectra, proton nuclear magnetic resonance (1H-NMR), thermogravimetric analysis, and transmission electron microscopy (TEM). FTIR spectral data revealed that Q acts as a bidentate ligand (chelating ligand) through carbonyl C(4) = O oxygen and phenolic C(3)-OH oxygen in conjugation with Zn. Electronic, FTIR, and 1H-NMR spectral data revealed that the Q/Zn complex has a distorted octahedral geometry, with the following chemical formula: [Zn(Q)(NO3)(H2O)2].5H2O. Diabetes was induced by streptozotocin (STZ) injection. A total of 70 male albino rats were divided into seven groups: control, diabetic untreated group and diabetic groups treated with either MSCs and/or Q and/or Q/Zn or their combination. Serum insulin, glucose, C-peptide, glycosylated hemoglobin, lipid profile, and enzymatic and non-enzymatic antioxidant levels were determined. Pancreatic and lung histology and TEM for pancreatic tissues in addition to gene expression of both SOD and CAT in pulmonary tissues were evaluated. MSCs in combination with Q/Zn therapy exhibited potent protective effects against STZ induced hyperglycemia and suppressed oxidative stress, genotoxicity, glycometabolic disturbances, and structural alterations. Engrafted MSCs were found inside pancreatic tissue at the end of the experiment. In conclusion, Q/Zn with MSC therapy produced a synergistic effect against oxidative stress and genotoxicity and can be considered potential ameliorative therapy against diabetes with pulmonary dysfunction, which may benefit against COVID-19.
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Diabetes Mellitus Experimental/terapia , Hipoglicemiantes/uso terapêutico , Transplante de Células-Tronco Mesenquimais , Quercetina/uso terapêutico , Zinco/uso terapêutico , Animais , Glicemia/análise , Glicemia/metabolismo , Peptídeo C/sangue , Peptídeo C/metabolismo , Células Cultivadas , Complexos de Coordenação/química , Complexos de Coordenação/uso terapêutico , Diabetes Mellitus Experimental/sangue , Diabetes Mellitus Experimental/metabolismo , Diabetes Mellitus Experimental/patologia , Hemoglobinas Glicadas/análise , Hemoglobinas Glicadas/metabolismo , Hiperglicemia/sangue , Hiperglicemia/metabolismo , Hiperglicemia/patologia , Hiperglicemia/terapia , Hipoglicemiantes/química , Insulina/sangue , Insulina/metabolismo , Pulmão/efeitos dos fármacos , Pulmão/metabolismo , Pulmão/patologia , Masculino , Estresse Oxidativo/efeitos dos fármacos , Quercetina/análogos & derivados , Ratos , Zinco/químicaRESUMO
This study aimed to evaluate the effect of daily sublethal doses of aluminum (Al) on hematological, physiological, biochemical, and behavioral changes in male albino Wistar rats. In addition, Al tissue accumulation and histopathological changes in the cerebral cortex, liver, and kidney were examined. The rats were randomly separated into three groups. Group 1 included rats who received the median deadly dose (LD50) of aluminum chloride (AlCl3), group 2 served as the control, and group 3 was treated with a non-lethal dose of AlCl3 (1.5 mg/kg) intraperitoneally for 45 days. At defined time intervals, hepatic and renal specific enzymes and biochemical activity were measured. In addition, we examined Al accumulation, the condition of the liver via histological methods, and the impact on the cerebral cortex. In comparison to the controls, rats treated with AlCl3 exhibited a rise in AST, ALT, and ALP enzyme activity. We also saw a significant decrease in body weight and a decrease in total protein, lipids, cholesterol, acetylcholinesterase (AChE), RBCs, and Hb levels compared to the control group. Histopathological examination suggested severe changes in the liver, kidney, and cerebral cortex of the rats. The current study indicates that sublethal daily exposure to AlCl3 causes hazardous effects, as increased Al concentration in the body is shown to induce detrimental biochemical and histological changes as well as decreased body weight. Therefore, careful attention should be given to treatments requiring long exposure in patients and the potential for accumulation via food and drinking.
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Cloreto de Alumínio/toxicidade , Córtex Cerebral/efeitos dos fármacos , Rim/efeitos dos fármacos , Fígado/efeitos dos fármacos , Animais , Peso Corporal/efeitos dos fármacos , Córtex Cerebral/metabolismo , Córtex Cerebral/patologia , Rim/metabolismo , Rim/patologia , Fígado/metabolismo , Fígado/patologia , Masculino , Estresse Oxidativo/efeitos dos fármacos , Ratos , Ratos WistarRESUMO
The present work aimed to assess the chondroprotective influence of chitosan and lecithin in a monoiodoacetate (MIA)-induced experimental osteoarthritis (OA) model. Forty male rats weighing 180-200 g were randomly distributed among the following five experimental groups (eight per group): control, MIA-induced OA, MIA-induced OA + chitosan, MIA-induced OA + lecithin, and MIA-induced OA + chitosan + lecithin. The levels of TNF-α, IL6, RF, ROS, and CRP, as well as mitochondrial markers such as mitochondrial swelling, cytochrome C oxidase (complex IV), MMP, and serum oxidative/antioxidant status (MDA level) (MPO and XO activities) were elevated in MIA-induced OA. Also, SDH (complex II) activity in addition to the levels of ATP, glutathione (GSH), and thiol was markedly diminished in the MIA-induced OA group compared to in control rats. These findings show that mitochondrial function is associated with OA pathophysiology and suggest that chitosan and lecithin could be promising potential ameliorative agents in OA animal models. Lecithin was more effective than chitosan in ameliorating all of the abovementioned parameters.
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Quitosana/farmacologia , Ácido Iodoacético/farmacologia , Lecitinas/farmacologia , Osteoartrite/induzido quimicamente , Osteoartrite/tratamento farmacológico , Trifosfato de Adenosina/metabolismo , Animais , Antioxidantes/metabolismo , Modelos Animais de Doenças , Complexo IV da Cadeia de Transporte de Elétrons/metabolismo , Glutationa/metabolismo , Interleucina-6/metabolismo , Masculino , Metaloproteinases da Matriz/metabolismo , Osteoartrite/metabolismo , Ratos , Espécies Reativas de Oxigênio/metabolismo , Fator de Necrose Tumoral alfa/metabolismoRESUMO
BACKGROUND: Selenium has a protective antioxidant effect on several tissues. Monosodium glutamate (MSG), MSG has been known as flavor enhancer that influences reversely on male reproductive systems and having a number of side effects, including reproductive toxicity. OBJECTIVES: The current study aims to evaluate the possible ameliorative functions of selenium nanoparticles (SeNPs) on MSG-induced reproductive toxicity. MATERIALS AND METHODS: In total, 42 male mice included in this study were divided into six groups: control, MSG (LD), MSG (HD), SeNPs, MSG (LD) plus SeNPs and finally MSG (HD) plus SeNPs. Testosterone hormone, tumor necrosis factor-alpha (TNF-α), as well as the antioxidant biomarkers: superoxide dismutase [SOD], glutathione peroxidase [GPx], catalase [CAT] and marker of lipid peroxidation [MDA], were examined. Histological and comet assay variations in the testicular tissues as markers of testicular damage after the MSG administration in two doses (MSG-LD and MSG-HD) either alone or combined with SeNPs.MSG in two doses (LD and HD) genotoxic effects were also evaluated and the ameliorative role of SeNPs on the testicular tissues were recorded. RESULTS: Results proved that the administration of SeNPs diminished the effect of MSG (LD and HD)-that induced decrease in testosterone hormone levels and elevated oxidative stress markers markedly. SeNPs had a potent antioxidant effect and elevated the antioxidant enzymes significantly and decreased lipid peroxidation markers as compared with MSG either (LD and HD) groups. CONCLUSION: It is clear from the data that SeNPs inhibit testicular injury and improve the antioxidant state in male mice.
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Fipronil (FPN), a phenylpyrazole insecticide, has been receiving increased attention owing to its toxicity, which is largely mediated through its effects on antioxidant systems. The present study was undertaken to assess the effects of resveratrol (RSV) and curcumin (CUR) on oxidative damage induced by FPN. Forty mature male Wistar rats were randomized into five groups (n = 8 per group): the first group was the control; the second was administered FPN (10 mg/kg); and the third, fourth, and fifth were co-treated with RSV (10 mg/kg), CUR (200 mg/kg), and their combination, respectively, 2 h prior to FPN administration. All animals were dosed via oral gavage for 4 weeks. FPN significantly (p < 0.05) elevated the sera of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), γ-glutamyl transferase (GGT), urea, creatinine, and cholesterol levels, whereas serum total protein, albumin, and triglyceride levels were significantly (p < 0.05) decreased, compared to those of the control group. Reduced glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) were decreased (p < 0.05) in the FPN-treated group compared to those in the control group; however, malondialdehyde (MDA) and nitric oxide (NO) levels were markedly increased (p < 0.05) in the hepatic, renal, and brain tissues. Co-treatment with RSV or CUR alleviated (p Ë 0.05) the increased lipid peroxidation and changes in enzymatic/nonenzymatic antioxidants induced by FPN; all these variables mostly returned to normal levels with the combined of RSV and CUR treatment. In conclusion, RSV and/or CUR relieved and synergistically reversed the FPN-induced tissue oxidative injury, probably by improving the antioxidant defenses via their free radical scavenging and antioxidant characteristics.
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Antioxidantes/metabolismo , Curcumina/metabolismo , Estresse Oxidativo/fisiologia , Pirazóis/toxicidade , Resveratrol/metabolismo , Animais , Sinergismo Farmacológico , Glutationa , Peroxidação de Lipídeos , Fígado , Masculino , Estresse Oxidativo/efeitos dos fármacos , Ratos , Ratos WistarRESUMO
Cadmium (Cd) has been reported to reduce male fertility, impair reproductive capacity, and play a major role in the pathogenesis of infertility. This study was conducted to investigate the possible protective role of Selenium (Se) and L-carnitine (LC) against the adverse effects induced by Cd on the male reproductive system in mice. Animals were randomly divided into seven groups (n = 10); control group and six treated groups, as follows: Cd (0.35 mg/kg), Se (0.87 mg/kg), LC (10 mg/kg), and a combination of either Se or LC and then a combination of both with Cd, and all animals were injected for a period of 30 days. Exposure of Cd showed a significant decrease in enzymatic antioxidant activities, deficiency in reproductive performance, decrease serum testosterone level, severe changes in the histopathological architecture, and higher degree of damages and appearance of unblemished DNA strands. Treatment with Se and LC has the highly synergistic and ameliorates the damaging effect of Cd on the testis through the elevation of the enzymatic antioxidant and diminish histopathological abnormalities and DNA damage.
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Selênio , Animais , Antioxidantes/metabolismo , Cádmio/metabolismo , Cádmio/toxicidade , Carnitina/farmacologia , Masculino , Camundongos , Estresse Oxidativo , Selênio/metabolismo , Selênio/farmacologia , Testículo/metabolismoRESUMO
BACKGROUND: Zinc oxide nanoparticles (ZnO NPs) are robustly used biomedicine. Moreover, no study has been conducted to explore the consequence of green synthesis of ZnO NPs with Camellia sinensis (green tea extract, GTE) on kidneys of rats treated with monosodium glutamate (MSG). METHODS: Therefore, the objective of the research was designed to explore the possible defensive effect of GTE/ZnO NPs against MSG-induced renal stress investigated at redox and histopathological points. RESULTS: The levels of urea and creatinine increased as the effect of a high dose of MSG, in addition, the myeloperoxidase and xanthine oxidase activates were elevated significantly with the high dose of MSG. The levels of non-enzymatic antioxidants (uric acid, glutathione, and thiol) were decreased sharply in MSG-treated rats as compared to the normal group. CONCLUSION: The data displayed that GTE/ZnO NPs reduced the effects of MSG significantly by reduction of the level peroxidation and enhancement intracellular antioxidant. These biochemical findings were supported by histopathology evaluation, which showed minor morphological changes in the kidneys of rats.
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Antioxidantes/metabolismo , Camellia sinensis/química , Rim/efeitos dos fármacos , Nanopartículas/química , Glutamato de Sódio/toxicidade , Óxido de Zinco/farmacologia , Animais , Biomarcadores/sangue , Glutationa/metabolismo , Rim/metabolismo , Rim/patologia , Testes de Função Renal , Oxirredução , Estresse Oxidativo/efeitos dos fármacos , Extratos Vegetais/química , Ratos Wistar , Glutamato de Sódio/metabolismo , Óxido de Zinco/químicaRESUMO
L-carnitine (LC) and selenium (Se) have significant protective and antioxidant effects on several tissues. Cadmium (Cd), widely used in some industries and emitted from fossil fuels, is a heavy metal having a number of side effects, including hepatotoxicity. This study aims to assess the ameliorative function of both LC and SeCl4 on cadmium chloride (CdCl2)-induced liver toxicity. In total, 70 male mice included in this study were allocated to seven groups: control, CdCl2, LC, SeCl4, CdCl2 plus SeCl4, CdCl2 plus LC, CdCl2 plus SeCl4 and LC groups. Hepatic aminotransferase (aspartate aminotransferase [AST] and alanine transaminase [ALT]) activity and tumor necrosis factor-alpha [TNF-α] levels, as well as the antioxidant biomarkers (superoxide dismutase [SOD], glutathione reductase [GRx], glutathione-S-transferase [GST] and catalase [CAT], were examined. Histological and transmission electron microscopic [TEM] variations in the liver were used as indicators of liver damage after the administration of CdCl2-alone or CdCl2 with LC, SeCl4, or both. Genotoxic effects of CdCl2 were also evaluated and the possible roles of SeCl4 and/or LC on the expression of the antioxidant enzymes were studied. Results showed that administration of LC and SeCl4 decreased CdCl2-induced increase in ALT and AST levels and reduced oxidative stress to normal levels. In addition, LC combined with SeCl4 had a highly synergistic effect and elevated significantly the enzymatic antioxidants and decreased lipid peroxidation levels compared with those in the CdCl2-treated group. It is clear from the data that both LC and SeCl4 inhibit liver injury and improve the redox state in mice.
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Anticarcinógenos/uso terapêutico , Antioxidantes/uso terapêutico , Cloreto de Cádmio/toxicidade , Carnitina/uso terapêutico , Doença Hepática Induzida por Substâncias e Drogas/tratamento farmacológico , Selênio/uso terapêutico , Alanina Transaminase/metabolismo , Animais , Anticarcinógenos/farmacologia , Antioxidantes/farmacologia , Apoptose/efeitos dos fármacos , Aspartato Aminotransferases/metabolismo , Carnitina/farmacologia , Catalase/metabolismo , Doença Hepática Induzida por Substâncias e Drogas/metabolismo , Glutationa Redutase/metabolismo , Glutationa Transferase/metabolismo , Peroxidação de Lipídeos/efeitos dos fármacos , Fígado/efeitos dos fármacos , Fígado/metabolismo , Masculino , Camundongos , Estresse Oxidativo/efeitos dos fármacos , Selênio/farmacologia , Superóxido Dismutase/metabolismoRESUMO
Background Aspartame (ASP) is used for treatment of obesity and diabetes mellitus. This study was designed to illustrate the biochemical responses and histopathological alterations besides the genotoxicity of ASP alone or with l-carnitine (LC) in the liver of rats. Methods Animals were separated into six groups: control, lower dose of ASP (ASP-LD; 75 mg/kg), higher dose of ASP (ASP-HD; 150 mg/kg), l-carnitine (LC; 10 mg/kg), ASP-LD plus LC, and ASP-HD plus LC. Treatment was carried out orally for 30 consecutive days. Results ASP raised the activity of some enzymes of liver markers and disturbed the lipid profile levels. The hepatic reduced glutathione (GSH) levels, the marker enzymes of antioxidant activities, were obviously diminished, and, possibly, the lipid peroxidation, C-reactive protein, and interleukins levels were increased. ASP significantly increased the DNA deterioration in comparison with the control in a dose-dependent manner. LC prevented ASP-induced liver damage as demonstrated by the enhancement of all the above parameters. Results of histopathological and electron microscopic examination proved the biochemical feedback and the improved LC effect on liver toxicity. Conclusions The co-treatment of LC showed different improvement mechanisms against ASP-induced liver impairment. So, the intake of ASP should be regulated and taken with LC when it is consumed in different foods or drinks to decrease its oxidative stress, histopathology, and genotoxicity of liver.
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Aspartame/toxicidade , Carnitina/farmacologia , Fígado/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Animais , Antioxidantes/metabolismo , Aspartame/administração & dosagem , Proteína C-Reativa/metabolismo , Relação Dose-Resposta a Droga , Glutationa/metabolismo , Interleucinas/metabolismo , Metabolismo dos Lipídeos/efeitos dos fármacos , Peroxidação de Lipídeos/efeitos dos fármacos , Fígado/patologia , Masculino , Microscopia Eletrônica/métodos , Testes de Mutagenicidade , RatosRESUMO
AIM: Melatonin (MLT) is a major hormone secreted by the pineal gland. In this study, a gold(III) MLT (Au+3/MLT) complex has been synthesized and investigating its protective effects against testicular damage. METHODOLOGY: The structural features of the complex were investigated. For biological assessment, 30 male rats were divided into three groups for 30 days. The first control group, the second received MLT and the third received Au+3/MLT complex. RESULTS: The Au+3/MLT complex was found to be nonelectrolytic with formula (Au[MLT]2[Cl][H2O]). The ligand is monodentate and adopt square-planar geometry. Its particles range in diameter from 35 to 100 nm. MLT affords slight oxidative stress protection. The Au+3/MLT complex significantly decreases TNF-α and IL-1ß levels but elevates antioxidant enzyme capacities, reducing lipid peroxidation markers and improving testicular histological structure. CONCLUSION: The Au+3/MLT complex improves the anti-inflammatory actions of MLT, exhibits potent antioxidant activity and enhances reproductive capacity.
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Anti-Inflamatórios/síntese química , Complexos de Coordenação/farmacologia , Ouro/química , Melatonina/química , Nanoestruturas/química , Testículo/efeitos dos fármacos , Animais , Anti-Inflamatórios/química , Anti-Inflamatórios/farmacologia , Antioxidantes/metabolismo , Catalase/metabolismo , Complexos de Coordenação/síntese química , Complexos de Coordenação/química , Interleucina-1beta/metabolismo , Magnetismo , Masculino , Modelos Animais , Ratos , Ratos Wistar , Superóxido Dismutase/metabolismo , Testículo/metabolismo , Testículo/patologia , Fator de Necrose Tumoral alfa/metabolismoRESUMO
The α-lipoic acid is a soft material and useful for the potential biomedical applications. The study was aimed to assess the potency of α-lipoic acid (ALA) against the toxicity of dimethylnitrosamine (DMN) on spleen of mice by assessing the antioxidants, histopathological and ultrastructure changes. The experiment was achieved on six groups of male mice as following; groups 1, 2, 3, and 4 were served as a control, ALA groups, low dose of DMN (DMN-LD; 2mgkg-1) and high dose of DMN (DMN-HD; 4mgkg-1). Group 5 was received DMN-LD plus ALA and group 6 was given DMN-HD plus ALA. The results indicated that DMN elevated lipid peroxidation, xanthine oxidase, nitric oxide, and decline the antioxidant enzymes as well as raise the C-reactive protein and tumor necrosis factor. A critical obstruction was harmonized with a reduced in lymphocyte number in the white pulp were observed. All the lymphatic nodules appeared smaller in DMN-HD group. In spleen tissues, marked changes of rough endoplasmic reticulum and appearance of three large lymphocytes were noticed. ALA/DMN treatments were improved all the oxidative damage and the ultrastructure changes. The data evince that ALA was eliminated the adverse effects of DMN on spleen of mice.
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Antioxidantes/farmacologia , Dimetilnitrosamina/toxicidade , Baço/efeitos dos fármacos , Baço/ultraestrutura , Ácido Tióctico/farmacologia , Animais , Peroxidação de Lipídeos/efeitos dos fármacos , Peroxidação de Lipídeos/fisiologia , Masculino , Camundongos , Baço/metabolismoRESUMO
Male albino rats of Wistar strain were injected intraperitoneally with nicotine or/and resveratrol for 4 weeks. Serum Interleukin-2, Interleukin-6, alpha-fetoprotein and tumor necrosis-alpha, as well as plasma 8-hydroxydeoxyguanosine of nicotine-treated rats were increased significantly. Myeloperoxidase, xanthine oxidase, nitric oxide, lipid peroxidation and total oxidative status of the lung in nicotine-treated rats were increased significantly, which were brought down to normal in resveratrol co-treated group. Endogenous antioxidant status as the activity of superoxide dismutase, catalase, glutathione peroxidase, and glucose-6-phosphate dehydrogenases were found to be decreased significantly in the lung of the nicotine-treated group, which were significantly raised in resveratrol-administered groups. The non-enzymatic antioxidants as total antioxidant and thiol levels were decreased significantly as the effect of nicotine that was effectively enhanced by resveratrol treatment. The lung of nicotine-treated rats showed severe congestion of the alveolar lung tissues with scattered congestion per bronchiolar and perivascular cells, as well as, inflammatory cells were observed. The data suggested that resveratrol exerts its protective effect by modulating the extent of oxidative status and improving the enzymatic/non-enzymatic antioxidant defense system, moreover, decreases the pathological changes in animals against the lung damage caused by nicotine.
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BACKGROUND: This study investigated whether the combination of sodium valproate (SV) with L-cysteine (LC) can decrease the SV toxicity of kidneys. SV caused alternation in oxidative/antioxidant balance. METHODS: Biochemical estimations included the determination of oxidative stress markers like thiobarbituric acid-reactive substances in kidney tissue, and enzymatic antioxidant activities such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase as well as total antioxidant capacity were evaluated in renal tissues. Creatinine and uric acid levels in the serum were also determined to assess kidney function. Pathological examination of the kidney was also performed. RESULTS: Increasing the levels of lipid peroxidation and decreasing the enzymatic activity (SOD, CAT, and GPx) as well as total antioxidant capacity of rats was shown with different doses of SV. Impairment in renal function tests suggests a decreased glomerular filtration rate, as serum creatinine was elevated. Histopathological changes of kidney tissue treated with SV reveal the proximal and the distal convoluted tubules that show hydropic changes (small white vacuoles within the cytoplasm and the glomeruli show hypercellularity). CONCLUSIONS: The concurrent administration of LC with SV significantly had beneficial effects on the kidney and all the above parameters have been improved.
Assuntos
Cisteína/farmacologia , Rim/efeitos dos fármacos , Substâncias Protetoras/farmacologia , Ácido Valproico/efeitos adversos , Animais , Antioxidantes/metabolismo , Biomarcadores/metabolismo , Catalase/metabolismo , Creatinina/metabolismo , Glutationa/metabolismo , Glutationa Peroxidase/metabolismo , Glutationa Redutase/metabolismo , Testes de Função Renal/métodos , Peroxidação de Lipídeos/efeitos dos fármacos , Masculino , Estresse Oxidativo/efeitos dos fármacos , Ratos , Superóxido Dismutase/metabolismo , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismoRESUMO
A new silver-carbocysteine (Ccy-Ag) complex [Ag2(Ccy)2(H2O)2] has been synthesized and characterized by using a combination of FTIR, Raman, molar conductivity, (1)H NMR, electronic spectra, thermal analyses, X-ray powder diffraction (XRD) and scanning electron microscopy (SEM). The infrared spectrum of Ccy-Ag complex in comparison with carbocysteine ligand prove that Ccy behaves as monobasic bidentate chelate to the silver metal ions via the deprotonated carboxylate O atom. The assessments of Ccy and its complexation with Ag(+) in treating COPD, evaluating immune activities through measuring IL-8, TGF-ß1, VEGF and TNF-α, antioxidant activities of (Ccy-Ag) complex by measuring SOD, MDA and GPX and bronchial asthma were discussed.