Some basic research has shown that nanomaterials can aggravate allergic asthma. However, its potential mechanism is insufficient. Based on the research that alumina nanopowder (nAl2O3) has been reported to cause lung tissue damage, the purpose of this study was to explore the relationship between nAl2O3 and allergic asthma as well as its molecular mechanism. In this study, Balb/c mice were sensitized with ovalbumin (OVA) to construct the allergic asthma model while intratracheally administered 0.5, 5 or 50 mg kg−1·day−1 nAl2O3 for 3 weeks. It was observed that exposure to nAl2O3 exacerbated airway hyperresponsiveness (AHR), airway remodeling, and inflammation cell infiltration, leading to lung function damage in mice. Results revealed that nAl2O3 could increase ROS levels and decrease GSH levels in lung tissue, promote the increases of the T-IgE, TGF-β, IL-1β and IL-6 levels, stimulate the overexpression of transcription factors GATA-3 and RORγt, decrease the levels of IFN-γ and IL-10 and increase the levels of IL-4 and IL-17A, resulting in the imbalance of Th1/Th2 and Treg/Th17 immune responses. In addition, antioxidant Vitamin E (Vit E) could alleviate asthma-like symptoms through blocking oxidative stress. The study displayed that exposure of nAl2O3 deteriorated allergic asthma through promoting the imbalances of Th1/Th2 and Treg/Th17.

In the present study we analyze the effect of seed treatment by a range of nano-TiO2 concentrations on the growth of Arabidopsis thaliana plants, on the vitamin E content and the expression of its biosynthetic genes, as well as activity of antioxidant enzymes and lipid peroxidation. To conduct the mechanistic analysis of nano-TiO2 on plants growth and antioxidant status we applied nanoparticles concentrations that are much higher than those reported in the environment. We find that as the concentration of nano-TiO2 increases, the biomass, and chlorophyll content in 5-week-old Arabidopsis thaliana plants decrease in a concentration dependent manner. In opposite, higher nano-TiO2 concentration enhanced root growth. Our results indicate that a high concentration of nano-TiO2 induces symptoms of toxicity and elevates the antioxidant level. We also find that the expression levels of tocopherol biosynthetic genes were either down- or upregulated in response to nano-TiO2. Thermoluminescence analysis shows that higher nano-TiO2 concentrations cause lipid peroxidation. To the best of our knowledge, this is the first report concerning the effect of nano-TiO2 on vitamin E status in plants. We conclude that nano-TiO2 affects the antioxidant response in Arabidopsis thaliana plants. This could be an effect of a changes in vitamin E gene expression that is diminished under lower tested nano-TiO2 concentrations and elevated under 1000 μg/ml.

The primary objective of this study was to understand the impact of monsoon and summer seasons on the Polychlorinated Biphenyls (PCB's) and petroleum hydrocarbon compounds (PHC's) load in Ennore estuary and how the physiological response of estuarine Scylla serrata inhabiting in this estuary changed with reference to antioxidant defense. Seasonal levels of PCB's and PHC's were assessed in the water along with their bioaccumulation in gills, hemolymph, hepatopancreas and ovary of S. serrata. Concentration of PCB's and PHC's in water and their bioaccumulation was found to be higher in summer season when compared to monsoon season. Enzymic antioxidant assays [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione reductase (GR), glutathione-S-transferase (GST)]; non-enzymic antioxidant assays [glutathione (GSH), vitamin C, vitamin E] and macromolecular alterations [membrane lipid peroxidation (LPO), and DNA Damage (strand breaks)] were assessed in the gills, hemolymph and hepatopancreas of S. serrata. There was a significant (p<0.05) upregulation in lipid peroxidation activity and DNA damage activity collected during the summer season when compared to the pre- and post-monsoon seasons. On the contrary, the enzymic and non-enzymic antioxidants exhibited significant (p<0.05) down regulation in the gills, hemolymph, hepatopancreas and ovary of S. serrata. Oxidative stress biomarkers represented a significant (p<0.05) maximum in gills when compared to hemolymph and hepatopancreas of S. serrata. Present study provided scientific evidences of how the antioxidant defense status of S. serrata responded to PCB's and PAH's stress with reference to seasonal vicissitudes, which indirectly represented the environmental health conditions of the estuary.

The protective effects of melatonin (Mel) and vitamin E (Vit E) against the negative effects of acetamiprid (Acmp) on testicles, reproductive hormones, and oxidative stress parameters were investigated in the present study. A total of 50 Balb-c male mice were used in 7 groups; 6 mice in the control groups (distilled water, corn oil, ethanol), and 8 in other groups (Acmp, Acmp + Mel, Acmp + Vit E, Acmp + Vit E + Mel). After the experiment, which lasted 21 days, hematoxylin eosin (H&E), periodic acid Schiff (PAS), and caspase-3 immunohistochemical (IHC) staining was performed on the testicular tissues. Also, the tissues were examined ultrastructurally with the transmission electron microscopy (TEM). In the Acmp group, there were decreased seminiferous tubule diameter and epithelial thickness, epithelial degeneration, decreased spermatozoa in the lumen, decreased PAS-positive staining in the seminiferous epithelial basement membrane, edema in the interstitial area, and hydropic degeneration in Leydig cells. Caspase-3 immunoreactivity was higher than in the other groups. TEM examination showed degeneration in tubule cells, lysosomal accumulation in cells of the spermatogenic line, vacuolizations with myelin figures, and necrosis. Hydropic degeneration, electron-dense lipid vacuoles, and chromatolysis were evident in the Leydig cell cytoplasm. In Sertoli cells, electron-dense lysosomal deposits were noted. In biochemical terms, there were decreased tissue glutathione (GSH) and total antioxidant status (TAS), and increased malondialdehyde (MDA) and total oxidant status (TOS). Plasma luteinizing hormone (LH), follicular stimulating hormone (FSH), and testosterone levels were decreased. In the groups with melatonin, vitamin E, and both were applied together, tissue damage, and apoptotic cell death were reduced at both light microscopic and ultrastructural levels. In biochemical terms, there were decreased oxidative parameters and increased hormonal parameters. It was found that vitamin E was more effective in decreasing oxidative parameters and increasing antioxidative parameters when compared to melatonin, and hormonal parameters increased at a higher level in the Acmp + Vit E group than in all groups. As a result, it was found that exposure to Acmp caused damage to testicular tissue, induced oxidative stress in testicles, and decreased plasma LH, FSH, and testosterone levels, and although vitamin E is more effective than melatonin in preventing this damage, both are effective.

Alzheimer’s disorder (AD) is very difficult to manage and treat. The complexity of the brain, the blood–brain barrier influencing a multitude of parameters/biomarkers, as well as numerous other factors involved often contribute to the decline in the chances of treatment success. Development of the new drug moiety also takes time, being necessary to consider both its toxicity and related issues. As a strategic plan, a combined strategy is being developed and considered to address AD pathology using several approaches. A combination of vitamin E, quercetin, and basil oil in a nano-based formulation is designed to be administered nasally. The antioxidant present in these natural-based products helps to treat and alleviate AD if a synergistic approach is considered. The three active substances mentioned above are well known for the treatment of neurodegenerative disorders. The nanoformulation helps the co-delivery of the drug moiety to the brain through the intranasal route. In this review, a correlation and use of vitamin E, quercetin, and basil oil in a nano-based formulation is described as an effective way to treat AD. The intranasal administration of drugs is a promising approach for the treatment of neurodegenerative and mental disorders, as this route is non-invasive, enhances the bioavailability, allows a drug dose reduction, bypasses the blood–brain barrier, and reduces the systemic undesired effect. The use of natural products is generally considered to be just as safe; therefore, by using this combined approach, the level of toxicity can be minimized.

Free radical or oxidative stress may be a fundamental mechanism underlying several human neurologic diseases. Therapy using free radical scavengers (antioxidants) has the potential to prevent, delay, or ameliorate many neurologic disorders. However, the biochemistry of oxidative pathobiology is complex, and optimum antioxidant therapeutic options may vary and need to be tailored to individual diseases. In vitro and animal model studies support the potential beneficial role of various antioxidant compounds in neurological disease. Antioxidants generally play an important role in reducing or preventing the cell damage and other changes which occur in the cells like mitochondrial dysfunction, DNA mutations, and lipid peroxidation in the cell membrane. Based on their mechanism of action, antioxidants can be used to treat various neurological disorders like Huntington’s disease, Alzheimer’s disease, and Parkinson’s disease. Vitamin E has a scavenging action for reactive oxygen species (ROS) and also prevents the lipid peroxidation. Creatine generally reduces the mitochondrial dysfunction in Parkinson’s disease (PD) patients. Various metal chelators are used in PD for the prevention of accumulation of the metals. Superoxidase dismutase (SOD), lipases, and proteases act as repair enzymes in patients with AD. Accordingly, the antioxidant defense system is found to be most useful for treating various neurological disorders.

Cisplatin (CP) is a highly effective chemotherapeutic agent against neoplasms, but its clinical utility is limited due to the side effects of its dose-dependent nephrotoxicity. Vitamin E (Vit E) and cod liver oil (CLO) are natural substances with chemoprotective effects. The present study was conducted to evaluate the protective effects of Vit E and/or CLO for CP-induced acute kidney injury (AKI) in rats. This study involved 40 mature male Wistar albino rats that were equally allocated into eight groups: Veh, Vit E, CLO, Vit E + CLO, CP, Vit E + CP, CLO + CP, and Vit E + CLO + CP. The co-administration of Vit E and CLO significantly ameliorated CP-induced elevations in serum creatinine (Cr), blood urea nitrogen (BUN), interleukin 1 beta (IL-1β), and interleukin- 6 (IL-6). Further, rats that received Vit E and/or CLO showed significant decrease in malondialdehyde (MDA) and increases in superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) levels in renal tissues, compared to CP-intoxicated rats. Additionally, the treatment restored the normal histological architecture (except for few cast formations) and upregulated the immunostaining area% of aquaporin 3 (AQP3) and downregulated the immunostaining area% of Bcl2 associated X protein (BAX) and inducible nitric oxide synthase (iNOS). The observed effects were stronger in the combination treatment group. The obtained data revealed that Vit E and CLO co-administration protects against the CP-induced AKI more than monotherapy with Vit E or CLO.

Arsenic toxicity becomes one of the major public health issues in several countries. Chronic and acute exposure to arsenic has been reported to be toxic to various systems of the human body and also observed in controlled experimental studies. The study was conducted to evaluate the neurotoxic effect of arsenic in Swiss albino mice and its amelioration by Vitamin E, Coenzyme Q10 and their combination. Swiss albino mice were treated with arsenic of 136 ppm for 15 days. The daily dose is 1/3 of LD 50 (acute) reported dose of arsenic. Thereafter, the animals were maintained either on drinking water or treated with Vitamin E (50 mg/kg bwt), Coenzyme Q10 (10 mg/kg bwt), and their combination by i.p.daily for 15 days. After the treatment, animals were sacrificed. The weight of the brain was marginally lower (ns), in arsenic-treated group as compared to control and antioxidant-protected groups. The LPO (lipid peroxidation) level was higher in arsenic-treated group, and this elevation was checked to some extent by the selected antioxidants which were statistically significant in combination of antioxidant-protected group. A significant reduction was found in GSH (reduced glutathione) level in the brain of arsenic-treated mice whereas GSH level was considerably higher in antioxidant-protected groups. Further, total thiol and total protein level were lower in arsenic-treated group. However, total thiol was significantly higher in antioxidant-protected groups. CAT (catalase) activity was significantly lower while SOD (superoxide dismutase) activity was marginally lowered in arsenic-treated group, and it was slightly higher in antioxidant-protected groups. Further, reduction in AChE (acetylcholinesterase) and BChE (butyrylcholinesterase) and motor coordination activity were also observed in arsenic-treated groups. Whereas, a higher AChE, BChE, and motor coordination activity was observed in antioxidant-protected group. These data indicate a positive role of selected antioxidant against the toxicity of arsenic in the brain of mice.

The purpose of this study was to investigate, for the first time, the effects of Bifenthrin (Bif) chronic exposure on plasmatic and aortic lipid parameters disturbance and their pro-atherogenic possibility in Wistar rats. The ameliorative role of vitamin E (Vit E) and selenium (Se) were also targeted. Thus, rats were treated by gastric gavage with combination of Vit E (100 mg/kg/bw) and Se (0.25 mg/kg/bw) in alone and co-treated groups for 90 days. Apart from control and Vit E-Se groups, all the groups were subjected to Bif (3 mg/kg, via gavage) toxicity. Results showed that Bif increased markedly plasmatic and aortic total cholesterol, LDL-cholesterol, native LDL-apoB-100, and oxidized-LDL, compared to the control. Moreover, Bif treatment significantly increased the plasmatic levels of the pro-inflammatory cytokines TNF-α, IL-2, and IL-6. In addition, the densitometric quantification of protein bands showed that the amount of hepatic native LDL-receptor protein decreased significantly in the intoxicated rats compared to the control group. The expression of arterial LDL receptors (LDLRs) and scavenger receptors (CD36) was amplified owing to Bif toxicity. This harmful effect was confirmed by histological study using Oil-Red-O staining. Owing to their antioxidant capacities, Vit E and Se have maintained all the changes in plasma and aorta lipids and prevented the pro-atherogenic effect observed in Bif-treated animals.

Despite the fact that amphotericin B (AmB) is currently considered as the first choice for treatment of visceral leishmaniasis, it is associated with some side effects. This study was designed to investigate the protective effects of vitamins A and E against amphotericin B-induced adverse effects in the kidney and liver of rat. Thirty male Wistar rats aged 7–8 weeks and weighing around 200 g were randomly divided into five groups, each one containing six rats. The first to fifth groups received olive oil as the control groups, AmB, AmB + vitamin A, AmB + vitamin E, and AmB + vitamins A + E, respectively. Rats received vitamins by gavage (vitamin A, 1000 IU/kg and vitamin E, 100 IU/kg) and amphotericin B by injections (5.5 mg/kg body weight). The treatment was constantly continued for 5 days and days 7 and 21. At the end of the study, serum level of TAC, TOS, MDA, liver enzyme activity (ALT, AST, ALP, LDH), renal factors (urea, uric acid, and creatinine), lipid profile as well as histopathological changes of the liver and kidney were investigated. AmB significantly increased serum level of creatinine, urea, uric acid, ALP, TOS, MDA, and kidney and renal tissue damage (p < 0.05). Supplementation AmB with vitamins A and E alone or combination improved oxidative stress status, liver and renal tissue structure, and functional parameters and serum lipid profile. This study highlighted the effects of vitamin A and vitamin E on attenuation of amphotericin B-induced side effects on the kidney and liver of male Wistar rats. Combination of the two vitamins is more effective than either alone improving the oxidative stress status, serum lipid profile, or liver and renal tissue structure and functional parameters.