The aim of this study was to evaluate the effects of high fat diet with or without grape juice during the pregnancy on gestational weight gain, biochemical parameters, and oxidative stress in plasma and liver from Wistar rats. Forty-nine rats were divided into four groups: control diet group (CD), high fat diet (HFD), grape juice and control diet (PGJCD), and grape juice and high fat diet (PGJHFD). During the treatment the weight gain of the rats was tracked. They had free access to their respective diets during 42 days of treatment. After offspring weaning, the mother rats were euthanized and blood and liver were collected. The high fat diet increased the total cholesterol and triglycerides serum levels as well as carbonyl levels in the liver, however this diet reduced the high-density lipoprotein (HDL) and urea levels in serum. Grape juice consumption reduced gestational body weight gain. In liver, the juice consumption increased sulfhydryl levels and reduced the superoxide dismutase (SOD) activity and TBARS level, in serum the consumption reduced aspartate aminotransferase (AST) and TBARS. We can conclude that the consumption of a diet rich in fat can promotes harmful effects on health during pregnancy, however the consumption of grape juice seems to be an important alternative to prevent oxidative damages and to promote the improvement of health.
This study evaluated the effect of lacosamide (LCM) on biochemical and mitochondrial parameters after PTZ kindling in mice. Male mice were treated on alternative days for a period of 11 days with LCM (20, 30, or 40 mg/kg), saline, or diazepam (2 mg/kg), before PTZ administration (50 mg/kg). The hippocampi were collected to evaluate free radicals, the activities of superoxide dismutase (SOD), catalase (CAT), and the mitochondrial complexes I‐III, II, and II‐III, as well as Bcl‐2 and cyclo‐oxygenase‐2 (COX‐2) expressions. Hippocampi, blood, and bone marrow were collected for genotoxic and mutagenic evaluations. LCM 40 mg/kg increased latency and decreased percentage of seizures, only on the 3rd day of observation. The dose of 30 mg/kg only showed positive effects on the percentage of seizures on the 2nd day of observation. LCM decreased free radicals and SOD activity and the dose of 40 mg/kg were able to increase CAT activity. LCM 30 and 40 mg/kg improved the enzymatic mitochondrial activity of the complex I‐III and LCM 30 mg/kg improved the activity of the complex II. In the comet assay, the damage induced by PTZ administration was reduced by LCM 20 and 30 mg/kg. The dose of 20 mg/kg increased COX‐2 expression while the highest dose used, 40 mg/kg, was able to reduce this expression when compared to the group treated with LCM 20 mg/kg. Although LCM did not produce the antiepileptogenic effect in vivo, it showed the neuroprotective effect against oxidative stress, bioenergetic dysfunction, and DNA damage induced by the repeated PTZ administration.
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