Dietary supplementation with inosine-5′-monophosphate improves the functional, energetic, and antioxidant status of liver and muscle growth in pigs

Inosine 5′-monophosphate (5′-IMP) is an essential nucleotide for de novo nucleotide biosynthesis and metabolism of energy, proteins, and antioxidants. Nucleotides are conditionally essential, as they cannot be produced sufficiently rapidly to meet the needs of the body in situations of oxidative stress or rapid muscle growth. A deficient intake of nucleotides can result in decreased ATP and GTP synthesis and impaired metabolism. We demonstrated that supplementation of finishing pig diets with 5′-IMP reduces the relative weight of the liver, and increases oxygen consumption during mitochondrial respiration without changing the ADP/O ratio, indicating an increase in the respiratory efficiency of liver mitochondria. We also observed a reduction in liver lipid peroxidation and an increase in muscle creatine. Moreover, 5′IMP supplementation increases slaughter weight, lean meat yield, sarcomere length, and backfat thickness in finishing barrows, demonstrating influence on protein metabolism. We suggest that 5′-IMP supplementation increase the mitochondrial respiratory capacity when the liver metabolic activity is stimulated, enhances antioxidant defense, and promotes muscle growth in finishing barrows.

The Intervention and Mechanism of Action for Aloin against Subchronic Aflatoxin B1 Induced Hepatic Injury in Rats

As a class of difurancoumarin compounds with similar structures, aflatoxins (AF) are commonly found in the environment, soil, and food crops. AF pose a serious threat to the health of humans, poultry, and livestock. This study aimed to investigate the neuroprotective effect and detailed mechanism of aloin on hepatic injury induced by subchronic AFB1 in rats. The result showed that aloin could significantly inhibit the decrease in food intake, body weight growth, immune organ index, and serum albumin content caused by long-term AFB1 exposure. Meanwhile, aloin reduced the level of serum liver function and improved renal swelling and pathological changes of liver tissue. Aloin could also inhibit liver lipid peroxidation and improve liver antioxidant capacity. Further investigation revealed that aloin inhibited the activity and expression of hepatic CYP1A2 and CYP3A4 and down-regulated IL-1β expression in subchronic AFB1-induced liver injury rats. The above study demonstrated that aloin played an important role in blocking or delaying the development process of subchronic AFB1-induced hepatotoxicity. Therefore, aloin is considered to have a potential role as a protective agent against AFB1.

Effects and Mechanisms of Chitosan and ChitosanOligosaccharide on Hepatic Lipogenesis and Lipid Peroxidation, Adipose Lipolysis, and Intestinal Lipid Absorption in Rats with High-Fat Diet-Induced Obesity

Chitosan and its derivative, chitosan oligosaccharide (CO), possess hypolipidemic and anti-obesity effects. However, it is still unclear if the mechanisms are different or similar between chitosan and CO. This study was designed to investigate and compare the effects of CO and high-molecular-weight chitosan (HC) on liver lipogenesis and lipid peroxidation, adipose lipolysis, and intestinal lipid absorption in high-fat (HF) diet-fed rats for 12 weeks. Rats were divided into four groups: normal control diet (NC), HF diet, HF diet+5% HC, and HF diet+5% CO. Both HC and CO supplementation could reduce liver lipid biosynthesis, but HC had a better effect than CO on improving liver lipid accumulation in HF diet-fed rats. The increased levels of triglyceride decreased lipolysis rate, and increased lipoprotein lipase activity in the perirenal adipose tissue of HF diet-fed rats could be significantly reversed by both HC and CO supplementation. HC, but not CO, supplementation promoted liver antioxidant enzymes glutathione peroxidase and superoxide dismutase activities and reduced liver lipid peroxidation. In the intestines, CO, but not HC, supplementation reduced lipid absorption by reducing the expression of fabp2 and fatp4 mRNA. These results suggest that HC and CO have different mechanisms for improving lipid metabolism in HF diet-fed rats.

Reduced Liver Lipid Peroxidation in Subcellular Fractions Is Associated with a Hypometabolic State in Rats with Portacaval Anastomosis

A surgical connection between portal and inferior cava veins was performed to generate an experimental model of high circulating ammonium and hepatic hypofunctioning. After 13 weeks of portacaval anastomosis (PCA), hyperammonemia and shrinkage in the liver were observed. Low glycemic levels accompanied by elevated levels of serum alanine aminotransferase were recorded. However, the activity of serum aspartate aminotransferase was reduced, without change in circulating urea. Histological and ultrastructural observations revealed ongoing vascularization and alterations in the hepatocyte nucleus (reduced diameter with indentations), fewer mitochondria, and numerous ribosomes in the endoplasmic reticulum. High activity of hepatic caspase-3 suggested apoptosis. PCA promoted a marked reduction in lipid peroxidation determined by TBARs in liver homogenate but specially in the mitochondrial and microsomal fractions. The reduced lipoperoxidative activity was also detected in assays supplemented with Fe2+. Only discreet changes were observed in conjugated dienes. Fluorescent probes showed significant attenuation in mitochondrial membrane potential, reactive oxygen species (ROS), and calcium content. Rats with PCA also showed reduced food intake and decreased energy expenditure through indirect calorimetry by measuring oxygen consumption with an open-flow respirometric system. We conclude that experimental PCA promotes an angiogenic state in the liver to confront the altered blood flow by reducing the prooxidant reactions associated with lower metabolic rate, along with significant reduction of mitochondrial content, but without a clear hepatic dysfunction.

The protective effect of Nigella Sativa oil extract against neurotoxicity induced by Valproic acid

Nigella sativa (NS), commonly known as black cumin, has been used for medicinal purposes. Traditionally the seeds and its oil are used in several diseases. The greatest part of the remedial properties of this plant is due to the presence of thymoquinone (TQ) which is a major active chemical component of the essential oil. The current study performed to evaluate the effect of Nigella sativa Oil (NSO) extract on the neurotoxic and hepatotoxic potentials from Valproic acid (VPA) administration. Also we summarize recent findings emphasizing the role of main neurotoxic and hepatotoxic markers and oxidative stress in study’s case. Neurotoxicity was induced by VPA at dose of (500 mg/kg b.wt) by gastric intubation daily for 30 day. These rats received NSO extract was given orally at dose of (0.5 ml/kg b.wt) daily for 30 days after VPA administration. The current results revealed that NSO extract treatment ameliorated significantly the elevated levels of the neurotoxic and hepatotoxic biomarkers which elevated as a result to VPA administration. Moreover, NSO extract treatment ameliorated the non-enzymatic antioxidant, brain and liver lipid peroxidation (LPO) and glutathione (GSH) concentration and the enzymatic antioxidant, brain and liver catalase(CAT) activity.

Gender-related difference in liver injury induced by Dioscorea bulbifera L. rhizome in mice

The present study was undertaken to investigate the gender-related liver injury induced by Dioscorea bulbifera L. (DB), a traditional medicinal plant, in mice, and further explored its hepatotoxic chemical compound. Serum and liver tissue samples were collected at 0, 4, 8, 12 h, after mice were administrated orally with 640 mg/kg ethyl acetate extracts (EF) isolated from DB. After treatments, serum alanine transaminase (ALT) and aspartate transaminase (AST) activities were both significantly elevated. Liver lipid peroxidation (LPO) level increased, while glutathione amounts, glutathione- S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT) activities all decreased in the time-dependent manner. Further analysis demonstrated that ALT and AST activities in female mice were significantly lower than those in male. Meanwhile, liver glutathione amounts and CAT activity in female mice after giving EF for 12 h were both higher than those in male. Further, comparing the liver injury induced by Diosbulbin B isolated from DB with that induced by EF on the basis of chemical analysis for the amounts of Diosbulbin B in EF of DB, we found that Diosbulbin B could be the main hepatotoxic chemical compound in DB. Taken together, our results show that DB can induce gender-related liver oxidative stress injury in mice, and its main hepatotoxic chemical compound is Diosbulbin B, for the first time.