Vitamin E-Inhibited Phoxim-Induced Renal Oxidative Stress and Mitochondrial Apoptosis In Vivo and In Vitro of Piglets.

Exposure to phoxim at low levels caused bioaccumulation with neurotoxicity but also induced oxidative stress, tissue damage, and abnormal nutrient metabolism. This study described that vitamin E ameliorates phoxim-induced nephrotoxicity via inhibiting mitochondrial apoptosis. In vivo, 24 healthy piglets were treated with phoxim (0 mg/kg and 500 mg/kg) and vitamin E + phoxim (vitamin E + phoxim: 200 mg/kg + 500 mg/kg). In vitro, PK15 cells were treated with phoxim (0 mg/L and 1 mg/L) and vitamin E + phoxim (phoxim + vitamin E: 1 mg/L + 1 mg/L) for 12 h and 24 h. Our results indicated that accumulation of ROS, oxidative stress, and renal cell injury through stimulation of mitochondrial apoptosis resulted in phoxim-induced nephrotoxicity. Phoxim resulted in swollen mitochondria, blurred internal cristae, renal glomerular atrophy, and renal interstitial fibrosis. Vitamin E alleviated the adverse effects of phoxim by reducing ROS and improving antioxidant capacity in vivo and in vitro. Vitamin E significantly increased SDH in vitro (p < 0.01), while it decreased ROS, Bad, and cyto-c in vitro and SOD and CAT in vivo (p < 0.05). Vitamin E ameliorated phoxim-induced renal histopathologic changes, and mitochondria swelled. In addition, vitamin E regulates phoxim-induced apoptosis by alleviating oxidative damage to the mitochondria.

Changes in glucose metabolism and mRNA expression of IRS-2 in rats exposed to phoxim and the protective effects of vitamin E.

Research has shown that organophosphorus pesticides impair glucose homeostasis and cause insulin resistance and type 2 diabetes. The current study investigates the influence of phoxim on insulin signaling pathways and the protective effects of vitamin E. Phoxim (180 mg kg-1) and VE (200 mg kg-1) were administered orally to Sprague-Dawley rats over a period of 28 consecutive days. After exposure to phoxim, the animals showed glucose intolerance and hyperinsulinemia during glucose tolerance tests, and insulin tolerance tests demonstrated an impaired glucose-lowering effect of insulin. Phoxim increases the fasting glucose, insulin and cholesterol levels, as well as the liver hexokinase activity (HK) significantly while decreasing the high density lipoprotein (HDL) cholesterol, and glycogen content in the liver and skeletal muscles observably. Furthermore, we observed an increase of insulin resistance biomarkers and a decrease of insulin sensitivity indices. The insulin receptor substrate (IRS)-2 mRNA expressions of liver and skeletal muscles were down-regulated by phoxim, while the expression of IRS-1 showed no difference. There were no differences in triglycerides, LDL-cholesterol, and fasting glucose treated with phoxim. On the basis of biochemical and molecular findings, phoxim has been determined to impair glucose homeostasis through insulin resistance and insulin signaling pathway disruptions resulting in a reduced function of insulin in hepatocytes and muscles. VE supplementation reduced the fasting glucose, increased the glycogen content and HDL-cholesterol, but did not reduce the insulin resistance indices, when phoxim-treated rats were compared to VE supplemented rats. Overall, this study shows that vitamin E modifies the phoxim toxicity in rats only to a moderate degree.

Vitamin E alleviates phoxim-induced toxic effects on intestinal oxidative stress, barrier function, and morphological changes in rats.

Phoxim is an organic phosphorus pesticide that remains easily in the environment, such as human food and animal feed. The objective of this study was to explore the effect of vitamin E on phoxim-induced oxidative stress in the intestinal tissues of Sprague-Dawley (SD) rats. Forty-eight Sprague-Dawley rats were randomly assigned to a control group and three treatment groups: treatment group 1 (phoxim: 20 mg/kg·BW), treatment group 2 (phoxim: 180 mg/kg·BW), and treatment 3 (vitamin E + phoxim: 200 mg/kg·BW + 180 mg/kg·BW). Phoxim was given by gavage administration once a day for 28 days. The results showed that phoxim significantly reduced jejunum villus height in rats (P < 0.05), and decreased the mRNA expression of junction protein genes of rats, including Occlidin and Claudin-4 (P < 0.05). Phoxim reduced GSH content and T-AOC level in the intestinal mucosa (P < 0.05). The mRNA expression levels of oxidative stress-related genes (Nrf2 and GPx2) were decreased. The mRNA expression of SOD was significantly increased. In addition, phoxim increased the level of interleukin-6 (IL-6) in jejunum mucosa and significantly reduced the level of IL-8 in ileum mucosas, while significantly increased TNF-α secretion. The mRNA expression levels of IL-1ß, IL-6, and IL-8 were significantly decreased, and mRNA expression of TNF-α was significantly increased (P < 0.05). Phoxim also increased the DNA expression of total cecal bacteria and Escherichia coli, inhibited the DNA expression of Lactobacillus and destroyed the intestinal barrier. Two hundred milligrams per kilogram BW vitamin E reduced the effect of phoxim on intestinal structure, alleviated the oxidative stress in intestinal tissue, and decreased the level of TNF-α. The mRNA expressions of antioxidative stress genes (SOD and GPx2) were significantly increased. The DNA expression level of Lactobacillus was significantly increased. In conclusion, vitamin E helped reduce the toxicity of organophosphate pesticides, such as phoxim on rat intestinal tissue.

Effects of dietary lecithin and l-carnitine on fatty acid composition and lipid-metabolic genes expression in subcutaneous fat and longissimus thoracis of growing-finishing pigs.

A 2×2 factorial experiment was conducted to investigate the effects of dietary lecithin and l-carnitine on fatty acid composition and lipid-metabolic genes expression in subcutaneous fat and longissimus thoracis of growing-finishing pigs. 160 barrows were assigned to 4 treatments consisting of 8 replicates with 5 pigs in each. The total PUFA, C18:2n-6 and C18:3n-3 in subcutaneous fat were increased by lecithin but the effect of lecithin was dependent of l-carnitine where supplementation of lecithin together with l-carnitine decreased total PUFA, C18:2n-6 and C18:3n-3. l-Carnitine increased the intramuscular fat content when supplemented with lecithin but no effect was observed without lecithin supplementation. l-Carnitine increased the mRNA expression of CPT1A, HSL, FABP4 and CRAT; and reduced the mRNA expression of FAS and ACCα in subcutaneous fat. Lecithin increased the mRNA expression of ACCα and ME1 in longissimus thoracis. l-Carnitine increased the mRNA expression of FAS in longissimus thoracis when supplemented with lecithin but no effect was observed without lecithin supplementation.

Dietary supplementation of l-arginine and chromium picolinate in sows during gestation affects the muscle fibre characteristics but not the performance of their progeny.

BACKGROUND: The present study investigated the effects of dietary supplementation of l-arginine and chromium picolinate (CrP) in sows during gestation on muscle fibre characteristics, performance and carcass characteristics of their progeny. Sixty healthy sows were randomly divided into four groups as a 2 × 2 factorial experiment design: one group received the control diet, another received the control diet + 10 g kg-1 l-arginine, the third group received the control diet + 400 ppb CrP, and the fourth group received the control diet + 10 g kg-1 l-arginine and 400 ppb CrP. RESULTS: The results showed that sows fed the diet supplemented with CrP produced progeny with higher muscle fibre numbers at birth, weaning and slaughter compared to sows fed the control diet. For mean fibre areas, the same result was found at weaning. For progeny of sows fed diets supplemented with l-arginine, only higher muscle fibre numbers at slaughter was observed. Almost no differences were observed regarding average daily gains, average daily feed intake, gain-to-feed ratios, carcass and meat traits. CONCLUSION: The results of the present study indicate that dietary supplementation of l-arginine and particularly CrP in sows during gestation alters muscle fibre numbers in their offspring, although not their performance or carcass characteristics. © 2017 Society of Chemical Industry.

Effects of phoxim-induced hepatotoxicity on SD rats and the protection of vitamin E.

Currently, public pay more attention to the adverse effect of organophosphate pesticides on human and animal health and on the environment in developing nations. Vitamin E may protect the hepatocyte and increase the function of liver. The study was to investigate the effects of phoxim-induced hepatotoxicity on Sprague Dawley (SD) rats and the protection of vitamin E. SD rats received by gavage 180 mg kg-1 (per body weight) of phoxim, 200 mg kg-1 (per body weight) of vitamin E, and phoxim + vitamin E. The results showed that exposure to phoxim elevated liver coefficient; glutamyl transpeptidase (GGT), aspartate aminotransferase, alkaline phosphatase, total bilirubin, total bile acid, and alanine aminotransferase in the serum; ROS in the liver; and the expression of p53, Bax, CYP2E1, ROS, caspase-9, caspase-8, and caspase-3, while phoxim caused a reduction of total protein, albumin, and cholinesterase in the serum; acetylcholinesterase, total antioxidant capacity, glutathione peroxidase, and glutathione in the liver; and the expression of Bcl-2. Vitamin E modified the phoxim-induced hepatotoxicity by reducing the GGT in the serum, malondialdehyde in the liver, and the expression of CYP2E1 significantly. There were no significant changes of globulin in the serum, the activity of catalase in the liver, as well as expression levels of Fas and Bad in the liver. Overall, subacute exposure to phoxim induced hepatic injury, oxidative stress damage, and cell apoptosis. Vitamin E modified phoxim-induced hepatotoxicity slightly. And, vitamin E minimized oxidative stress damage and ultrastructural changes in rat hepatocytes notably.