ß-Carotene Supplementation Improves Pancreas Function during Moderate Ethanol Consumption: Initial Characterization from a Morphological Overview.

Alcohol is believed to harm acinar cells, pancreatic ductal epithelium, and pancreatic stellate cells. After giving ethanol and/or ß-carotene to C57BL/6 mice, our goal was to evaluate their biochemistry, histology, and morpho-quantitative features. There were six groups of C57BL/6 mice: 1. Group C (control), 2. Group LA (low-dose alcohol), 3. Group MA (moderate-dose alcohol), 4. Group B (ß-carotene), 5. Group LA + B (low-dose alcohol combined with ß-carotene), and 6. Group MA + B (moderate-dose alcohol combined with ß-carotene). After the animals were euthanized on day 28, each specimen's pancreatic tissue was taken. Lipase, uric acid, and amylase were assessed using biochemical assessment. Furthermore, the examination of the pancreatic structure was conducted using Ammann's fibrosis scoring system. Finally, the morpho-quantitative characteristics of the pancreatic islets and acinar cells were determined. In the serum of the MA + B group, there were higher amounts of total amylase (825.953 ± 193.412 U/L) and lower amounts of lipase (47.139 ± 6.099 U/L) (p < 0.05). Furthermore, Ammann's fibrosis punctuation in the pancreas revealed significant variations between the groups (p < 0.001). Finally, the stereological analysis of pancreatic islets showed that the groups were different (p < 0.001). These findings suggest that antioxidant treatments might help decrease the negative effects of ethanol exposure in animal models.

ß-Carotene Increases Activity of Cytochrome P450 2E1 during Ethanol Consumption.

One of the key routes through which ethanol induces oxidative stress appears to be the activation of cytochrome P450 2E1 at different levels of ethanol intake. Our aim was to determine if oral ß-carotene intake had an antioxidant effect on CYP2E1 gene expression in mice that had previously consumed ethanol. C57BL/6 mice were used and distributed into: control (C), low-dose alcohol (LA), moderate-dose alcohol (MA), ß-carotene (B), low-dose alcohol+ß-carotene (LA + B), and moderate-dose alcohol+ß-carotene (MA + B). Animals were euthanized at the end of the experiment, and liver tissue was taken from each one. CYP2E1 was measured using qPCR to detect liver damage. The relative expression level of each RNA was estimated using the comparative threshold cycle (Ct) technique (2-ΔΔCT method) by averaging the Ct values from three replicates. The LA+B (2267 ± 0.707) and MA+B (2.307 ± 0.384) groups had the highest CYP2E1 fold change values. On the other hand, the C (1.053 ± 0.292) and LA (1.240 ± 0.163) groups had the lowest levels. These results suggest that ethanol feeding produced a fold increase in CYP2E1 protein in mice as compared to the control group. Increased CYP2E1 activity was found to support the hypothesis that ß-carotene might be dangerous during ethanol exposure in animal models. Our findings imply that ß-carotene can increase the hepatic damage caused by low and high doses of alcohol. Therefore, the quantity of alcohol ingested, the exposure period, the regulatory mechanisms of alcoholic liver damage, and the signaling pathways involved in the consumption of both alcohol and antioxidant must all be considered.

Resveratrol atenua o estresse oxidativo e a lesão muscular de ratos sedentários submetidos ao exercício físico / Resveratrol attenuates oxidative stress and muscle damage in sedentary rats subjected to physical exercise

O sedentarismo é um problema de saúde pública e um dos maiores males da sociedade moderna. Já está bem estabelecido que esforço físico em excesso ou em indivíduos não condicionados acarreta estresse oxidativo e lesões musculares. No presente estudo, foi testada a hipótese de que um único esforço físico é capaz de causar estresse oxidativo e lesão muscular em indivíduos sedentários. Aditivamente foi avaliado efeito antioxidante do polifenol resveratrol (RV) quanto a sua capacidade de atenuar o estresse oxidativo e a lesão muscular causados pelo esforço físico. Para tal, 40 ratos (Rattus norvegicus albinus, Wistar), machos, adultos e sedentários foram aleatoriamente submetidos ou não a 90 minutos de natação, com e sem tratamento com RV (100mg/kg/PV/14dias): N-RV- (n=10) grupo mantido em repouso e não tratado com RV; N-RV+ (n=10) grupo mantido em repouso e tratado com RV; N+RV- (n=10) grupo submetido ao esforço físico de natação e não tratado com RV e N+RV+ (n=10) grupo submetido ao esforço físico de natação e tratado com RV. Em ratos sedentários, o esforço físico da natação promoveu estresse oxidativo (aumento da peroxidação lipídica e diminuição da capacidade antioxidante total do plasma) e aumento significativo da atividade plasmática de creatina quinase (CK) e lactato desidrogenase (LDH). O tratamento com RV diminuiu a peroxidação lipídica e a concentração dos marcadores de lesão muscular (CK e LDH) de ratos sedentários submetidos à natação. Essa é uma das primeiras evidências de que um único esforço físico pode causar estresse oxidativo em indivíduos sedentários e que o RV pode ser uma alternativa para atenuar a lesão muscular causada por esse estresse.(AU)

Physical inactivity is a public health problem when a sedentary population practices physical activity sporadically. Exercise in unconditioned individuals causes oxidative stress and muscle damage. This study tested the hypothesis that a single physical exertion can cause muscle damage and oxidative stress in sedentary individuals, and resveratrol can attenuate it. For this, 40 sedentary adult male rats were equally and randomized into four groups subjected to 90min swimming or rest and administered aqueous resveratrol (100mg/kg/day) or saline for 14 days: N-RV-, rats maintained at rest and administered saline; N-RV+, rats maintained at rest and treated with resveratrol; N+RV-, rats subjected to physical exercise and administered saline; and N+RV+, rats subjected to physical exercise and treated with resveratrol. In sedentary rats, the physical exertion of swimming promoted oxidative stress, i.e. increased lipid peroxidation and decreased plasma total antioxidant capacity, and significant increases in CK and LDH plasma activities. Resveratrol diminished lipid peroxidation and the concentrations of muscle damage markers (CK and LDH) in sedentary rats subjected to swimming. The results provide evidence that a single sudden physical exertion can cause oxidative stress in sedentary rats. Resveratrol showed good results as a treatment for minimizing muscle damage caused by this stress.(AU)

Resveratrol atenua o estresse oxidativo e a lesão muscular de ratos sedentários submetidos ao exercício físico / Resveratrol attenuates oxidative stress and muscle damage in sedentary rats subjected to physical exercise

O sedentarismo é um problema de saúde pública e um dos maiores males da sociedade moderna. Já está bem estabelecido que esforço físico em excesso ou em indivíduos não condicionados acarreta estresse oxidativo e lesões musculares. No presente estudo, foi testada a hipótese de que um único esforço físico é capaz de causar estresse oxidativo e lesão muscular em indivíduos sedentários. Aditivamente foi avaliado efeito antioxidante do polifenol resveratrol (RV) quanto a sua capacidade de atenuar o estresse oxidativo e a lesão muscular causados pelo esforço físico. Para tal, 40 ratos (Rattus norvegicus albinus, Wistar), machos, adultos e sedentários foram aleatoriamente submetidos ou não a 90 minutos de natação, com e sem tratamento com RV (100mg/kg/PV/14dias): N-RV- (n=10) grupo mantido em repouso e não tratado com RV; N-RV+ (n=10) grupo mantido em repouso e tratado com RV; N+RV- (n=10) grupo submetido ao esforço físico de natação e não tratado com RV e N+RV+ (n=10) grupo submetido ao esforço físico de natação e tratado com RV. Em ratos sedentários, o esforço físico da natação promoveu estresse oxidativo (aumento da peroxidação lipídica e diminuição da capacidade antioxidante total do plasma) e aumento significativo da atividade plasmática de creatina quinase (CK) e lactato desidrogenase (LDH). O tratamento com RV diminuiu a peroxidação lipídica e a concentração dos marcadores de lesão muscular (CK e LDH) de ratos sedentários submetidos à natação. Essa é uma das primeiras evidências de que um único esforço físico pode causar estresse oxidativo em indivíduos sedentários e que o RV pode ser uma alternativa para atenuar a lesão muscular causada por esse estresse.(AU)

Physical inactivity is a public health problem when a sedentary population practices physical activity sporadically. Exercise in unconditioned individuals causes oxidative stress and muscle damage. This study tested the hypothesis that a single physical exertion can cause muscle damage and oxidative stress in sedentary individuals, and resveratrol can attenuate it. For this, 40 sedentary adult male rats were equally and randomized into four groups subjected to 90min swimming or rest and administered aqueous resveratrol (100mg/kg/day) or saline for 14 days: N-RV-, rats maintained at rest and administered saline; N-RV+, rats maintained at rest and treated with resveratrol; N+RV-, rats subjected to physical exercise and administered saline; and N+RV+, rats subjected to physical exercise and treated with resveratrol. In sedentary rats, the physical exertion of swimming promoted oxidative stress, i.e. increased lipid peroxidation and decreased plasma total antioxidant capacity, and significant increases in CK and LDH plasma activities. Resveratrol diminished lipid peroxidation and the concentrations of muscle damage markers (CK and LDH) in sedentary rats subjected to swimming. The results provide evidence that a single sudden physical exertion can cause oxidative stress in sedentary rats. Resveratrol showed good results as a treatment for minimizing muscle damage caused by this stress.(AU)

N-acetyl-cysteine inhibits liver oxidative stress markers in BALB/c mice infected with Leishmania amazonensis

BACKGROUND Leishmaniasis is a parasitosis caused by several species of the genus Leishmania. These parasites present high resistance against oxidative stress generated by inflammatory cells. OBJECTIVES To investigate oxidative stress and molecular inflammatory markers in BALB/c mice infected with L. amazonensis and the effect of antioxidant treatment on these parameters. METHODS Four months after infection, oxidative and inflammatory parameters of liver, kidneys, spleen, heart and lungs from BALB/c mice were assessed. FINDINGS In liver, L. amazonensis caused thiol oxidation and nitrotyrosine formation; SOD activity and SOD2 protein content were increased while SOD1 protein content decreased. The content of the cytokines IL-1β, IL-6, TNF-α, and the receptor of advanced glycation endproducts (RAGE) increased in liver. Treatment with the antioxidant N-acetyl-cysteine (20 mg/kg b.w) for five days inhibited oxidative stress parameters. MAIN CONCLUSIONS L. amazonensis induces significant alterations in the redox status of liver but not in other organs. Acute antioxidant treatment alleviates oxidative stress in liver, but it had no effect on pro-inflammatory markers. These results indicate that the pathobiology of leishmaniasis is not restricted to the cutaneous manifestations and open perspectives for the development of new therapeutic approaches to the disease, especially for liver function.

Inflammatory and oxidative stress in rotavirus infection.

Rotaviruses are the single leading cause of life-threatening diarrhea affecting children under 5 years of age. Rotavirus entry into the host cell seems to occur by sequential interactions between virion proteins and various cell surface molecules. The entry mechanisms seem to involve the contribution of cellular molecules having binding, chaperoning and oxido-reducing activities. It appears to be that the receptor usage and tropism of rotaviruses is determined by the species, cell line and rotavirus strain. Rotaviruses have evolved functions which can antagonize the host innate immune response, whereas are able to induce endoplasmic reticulum (ER) stress, oxidative stress and inflammatory signaling. A networking between ER stress, inflammation and oxidative stress is suggested, in which release of calcium from the ER increases the generation of mitochondrial reactive oxygen species (ROS) leading to toxic accumulation of ROS within ER and mitochondria. Sustained ER stress potentially stimulates inflammatory response through unfolded protein response pathways. However, the detailed characterization of the molecular mechanisms underpinning these rotavirus-induced stressful conditions is still lacking. The signaling events triggered by host recognition of virus-associated molecular patterns offers an opportunity for the development of novel therapeutic strategies aimed at interfering with rotavirus infection. The use of N-acetylcysteine, non-steroidal anti-inflammatory drugs and PPARγ agonists to inhibit rotavirus infection opens a new way for treating the rotavirus-induced diarrhea and complementing vaccines.