Anticancer Activity of Encapsulated Pearl Millet Polyphenol-Rich Extract against Proliferating and Non-Proliferating Breast Cancer Cells In Vitro.

Plant-derived polyphenols are bioactive compounds with potential health-promoting properties including antioxidant, anti-inflammatory, and anticancer activity. However, their beneficial effects and biomedical applications may be limited due to their low bioavailability. In the present study, we have considered a microencapsulation-based drug delivery system to investigate the anticancer effects of polyphenol-rich (apigenin, caffeic acid, and luteolin) fractions, extracted from a cereal crop pearl millet (Pennisetum glaucum), using three phenotypically different cellular models of breast cancer in vitro, namely triple negative HCC1806, ER-positive HCC1428, and HER2-positive AU565 cells. Encapsulated polyphenolic extract induced apoptotic cell death in breast cancer cells with different receptor status, whereas it was ineffective against non-tumorigenic MCF10F cells. Encapsulated polyphenolic extract was also found to be cytotoxic against drug-resistant doxorubicin-induced senescent breast cancer cells that were accompanied by increased levels of apoptotic and necrotic markers, cell cycle inhibitor p21 and proinflammatory cytokine IL8. Furthermore, diverse responses to the stimulation with encapsulated polyphenolic extract in senescent breast cancer cells were observed, as in the encapsulated polyphenolic extract-treated non-proliferating AU565 cells, the autophagic pathway, here cytotoxic autophagy, was also induced, as judged by elevated levels of beclin-1 and LC3b. We show for the first time the anti-breast cancer activity of encapsulated polyphenolic extract of pearl millet and postulate that microencapsulation may be a useful approach for potentiating the anticancer effects of phytochemicals with limited bioavailability.

Neuroprotective effects of magnesium against stress induced by hydrogen peroxide in Wistar rat.

INTRODUCTION: Oxidative stress has been implicated in the pathogenesis of diverse disease states. The present study was designed to examine the effects of magnesium sulphate (MgSO4) against hydrogen peroxide (H2O2) induced behaviour impairment and oxidative damage in rats. MATERIAL AND METHODS: Eighteen rats were equally divided into three groups. The first group was kept as a control. In the second group, H2O2 was given in drinking water at 3% during 5 days. In the third group, rats were subjected to daily administration of H2O2 and MgSO4 (100 mg/kg; b.w) for 5 days. Animals were subjected to behavioural tests (elevated plus maze and open field). At the end of experiment, brains were extracted for oxidative stress biomarkers assessment including levels of malondialdéhyde and hydrogen peroxide and activities of superoxide dismutase and catalase. RESULTS: Our findings showed that H2O2 treated rat exhibited anxiogenic behaviour and the genesis of free radicals in the brain. Magnesium showed amelioration against oxidative stress and significant decrease in anxiety levels. DISCUSSION AND CONCLUSION: Stress is a powerful process that disrupts brain homeostasis by inducing oxidative stress and its appear that magnesium may have potential therapeutic benefits by reducing oxidative stress and inducing anxiolytic effect.

Static magnetic field exposure-induced oxidative response and caspase-independent apoptosis in rat liver: effect of selenium and vitamin E supplementations.

In the present study, we investigated the implication of oxidative stress and apoptosis under static magnetic field (SMF) in the brain and liver. Moreover, we estimated the protective role of selenium and vitamin E in rat tissues against disorders induced by SMF. Exposure of rats to SMF (128 mT, 1 h/day during five consecutive days) increased the activity of catalase (CAT) (+24 %) in the liver but not in the brain. By contrast, the same treatment failed to alter malondialdehyde (MDA) concentration in the brain and liver. Exposure to SMF also induced hepatocyte apoptosis through a caspase-independent pathway involving mitochondrial apoptosis-inducing factor (AIF) but not in the brain. Selenium and vitamin E supplementations to SMF-exposed rats restored liver CAT activity but failed to minimize liver apoptosis.

Does static magnetic field-exposure induced oxidative stress and apoptosis in rat kidney and muscle? Effect of vitamin E and selenium supplementations.

Static magnetic fields (SMFs) effect observed with radical pair recombination is one of the well-known mechanisms by which SMFs interact with biological systems. Our aim was to study whether SMF induces oxidative stress and apoptosis in rat tissues and to evaluate the possible protector effect of selenium (Se) and vitamin E (vit E) supplementations. Rats were randomly divided into control, SMF-exposed, Se-treated, vit E-treated, SMF exposed rats and co-treated with Se, and SMF exposed rats and co-treated with vit E. After animal sacrifice, catalase (CAT) activity and malondialdehyde (MDA) concentration were measured and apoptosis inducing factor (AIF) immunohistochemical labeling was performed in kidney and muscle. Exposure of rats to SMF (128 mT, 1 h/day for 5 days) increased the MDA concentrations (+25%) and CAT activities (+34%) in kidney but not in muscle. By contrast, the same treatment failed to induce a caspase-independent pathway apoptosis in both tissues. Interestingly, Se pre-treatment inhibited the increase of MDA concentrations and CAT activities in kidney in SMF-exposed rats. However, vit E administration corrected only MDA levels in rat kidney. In conclusion, exposure to SMF induced oxidative stress in kidney that can be prevented by treatment with Se or vit E.

Vitamin D supplementation ameliorates hypoinsulinemia and hyperglycemia in static magnetic field-exposed rat.

The purpose of this study is to evaluate the effects of vitamin D supplementation on glucose and lipid metabolism in static magnetic field (SMF)-exposed rats. Rats exposed to SMF (128 mT; 1 h/day) during 5 consecutive days showed an increase in plasma glucose level and a decrease in plasma insulin concentration. By contrast, the same treatment failed to alter body weight and plasmatic total cholesterol, high-density lipoprotein (HDL)-cholesterol, low-density lipoprotein (LDL)-cholesterol, and triglyceride levels. Interestingly, supplementation with vitamin D (1,600 IU/100 g, per os) corrected and restored glycemia and insulinemia in SMF-exposed rats. The same treatment had no effects on lipid metabolism.

Vitamin E prevents glucose metabolism alterations induced by static magnetic field in rats.

In the present study, we investigate the effects of a possible protective role of vitamin E (vit E) or selenium (Se) on glucose metabolism disruption induced by static magnetic field (SMF) in rats. Rats have been exposed to SMF (128 mT, 1 h/day during 5 days). Our results showed that SMF failed to alter body weight and relative liver weight. Our data demonstrated that exposure to SMF increased (+21 %) blood glucose level and caused a decrease (-15 %) in liver glycogen content. Moreover, the same treatment induced a reduction of pancreatic islet area. Interestingly, supplementation with vit E (DL α-tocopherol acetate, 150 mg/kg per os during 5 days) prevented alterations induced by SMF on glucose metabolism and liver glycogen content, whereas supplementation with Se (Na2SeO3, 0.20 mg/l, in drinking water for 4 weeks) restored only hepatic glycogen contents. By contrast, both vit E and Se failed to correct the area of pancreatic islets.

Vitamins and glucose metabolism: The role of static magnetic fields.

PURPOSE: This review focuses on our own data and other data from the literature of static magnetic fields (SMF) bioeffects and vitamins and glucose metabolism. Three main areas of investigation have been covered: Static magnetic field and glucose metabolism, static magnetic field and vitamins and the role of vitamins on glucose metabolism. CONCLUSION: Considering these articles comprehensively, the conclusions are as follows: The primary cause of changes in cells after incubation in external SMF is disruption of free radical metabolism and elevation of their concentration. Such disruption causes oxidative stress leading to an unsteadiness of glucose level and insulin release. Moreover, based on available data, it was concluded that exposure to SMF alters plasma levels of vitamin A, C, D and E; these parameters can take part in disorder of glucose homeostasis and insulin release.

Bioeffects of static magnetic fields: oxidative stress, genotoxic effects, and cancer studies.

The interaction of static magnetic fields (SMFs) with living organisms is a rapidly growing field of investigation. The magnetic fields (MFs) effect observed with radical pair recombination is one of the well-known mechanisms by which MFs interact with biological systems. Exposure to SMF can increase the activity, concentration, and life time of paramagnetic free radicals, which might cause oxidative stress, genetic mutation, and/or apoptosis. Current evidence suggests that cell proliferation can be influenced by a treatment with both SMFs and anticancer drugs. It has been recently found that SMFs can enhance the anticancer effect of chemotherapeutic drugs; this may provide a new strategy for cancer therapy. This review focuses on our own data and other data from the literature of SMFs bioeffects. Three main areas of investigation have been covered: free radical generation and oxidative stress, apoptosis and genotoxicity, and cancer. After an introduction on SMF classification and medical applications, the basic phenomena to understand the bioeffects are described. The scientific literature is summarized, integrated, and critically analyzed with the help of authoritative reviews by recognized experts; international safety guidelines are also cited.

Selenium supplementation ameliorates static magnetic field-induced disorders in antioxidant status in rat tissues.

The aim of this study was to investigate the effect of selenium supplementation on the antioxidant enzymatic system (such as GPx, GR and SOD), GSH and selenium level in liver, kidney, muscle and brain of static magnetic field (SMF) exposed rats. Male adult rats were divided into control rats (n=6), SMF-exposed rats (128 mT; 1h/day for 5 days), selenium-treated rats (Na(2)SeO(3), 0.2mg/l, in drinking water for 4 weeks) and co-exposed rats (selenium for 4 weeks and SMF during the last 5 consecutive days). Sub-acute exposure to SMF induces a decrease of selenium levels in kidney, muscle and brain. Our results also revealed a decrease of GPx activities in kidney and muscle. By contrast, SMF exposure increased total GSH levels and total SOD activities in liver, while glutathione reductase activity is unaffected. Selenium supplementation in SMF-exposed rats restored selenium levels in kidney, muscle and brain and elevated the activities of GPx in kidney and muscle to those of control group. In the liver, selenium supplementation failed to bring down the elevated levels of total GSH and SOD activity. Our investigations suggested that sub-acute exposure to SMF altered the antioxidant response by decreasing the level of total selenium in kidney, muscle and brain. Interestingly, selenium supplementation ameliorates antioxidant capacity in rat tissues exposed to SMF.

Effect of selenium pre-treatment on plasma antioxidant vitamins A (retinol) and E (α-tocopherol) in static magnetic field-exposed rats.

In the present study, we evaluate the effect of the co-exposure to static magnetic field (SMF) and selenium (Se) on the antioxidant vitamins A and E levels and some other parameters of oxidative stress in rat. Sub-acute exposure of male adult rats to a uniform SMF (128 mT, 1 h/day during 5 consecutive days) increased plasma activity of glutathione peroxidase (+35%) but decreased α-tocopherol (-67%) and retinol levels (-41%). SMF exposure failed to alter the plasmatic thiobarbituric acid-reactive species (TBARs), total thiol groups and selenium concentrations. Sub-chronic administration of Se (Na(2)SeO(3), 0.2 mg/L, for 30 consecutive days, per os) ameliorated the antioxidant capacities in SMF-treated rats. Our investigation demonstrated that sub-acute exposure to SMF induced oxidative stress, which may be prevented by a pretreatment with selenium.

Time-dependent effects of exposure to static magnetic field on glucose and lipid metabolism in rat.

In the following study, we investigate the effects of static magnetic field (SMF) (128 mT, 1 h/day during 5 or 15 consecutive days) on anthropometric parameters, glucose and lipid metabolism in rats. Exposure to SMF during 5 days induced a decrease (-8%, p < 0.05) in relative liver weight and serum insulin concentration (-56%, p < 0.001), while blood glucose level was increased (+10%, p < 0.001). By contrast, the same treatment failed to alter body weight, relative kidney weight and levels of lactate, cholesterol, triglycerides and phospholipids. Exposure to SMF during 15 days induced a decrease (-15 %, p < 0.001) in body weight, liver weight (-15 %, p < 0.05), insulin concentration (-63%, p < 0.001), plasmatic lactate level (-55%, p < 0.05) and increased glucose (+24%, p < 0.001), cholesterol (+30%, p < 0.01,) and phospholipids levels (+58%, p < 0.001), whereas, triglycerides decreased (-28%, p < 0.001). These results showed that SMF effects on glucose and lipid metabolism are time-dependent.