Bacillus amyloliquefaciens B10 can alleviate liver apoptosis and oxidative stress induced by aflatoxin B1

The ability to respond to perturbations in endoplasmic reticulum (ER) function is a fundamentally important property of all cells, but ER stress can also lead to apoptosis. In settings of chronic ER stress, the associated apoptosis may contribute to pathophysiological processes involved in a number of prevalent diseases, including neurodegenerative diseases, diabetes, atherosclerosis and renal disease. The molecular mechanisms linking ER stress to apoptosis are the topic of this review, with emphases on relevance to pathophysiology and integration and complementation among the various apoptotic pathways induced by ER stress. © 2011 Macmillan Publishers Limited. All rights reserved

Oxidative stress and chronic inflammation are known to be associated with the development of metabolic diseases, including diabetes. Oxidative stress, an imbalance between oxidative and antioxidative systems of cells and tissues, is a result of over production of oxidative-free radicals and associated reactive oxygen species (ROS). One outcome of excessive levels of ROS is the modification of the structure and function of cellular proteins and lipids, leading to cellular dysfunction including impaired energy metabolism, altered cell signalling and cell cycle control, impaired cell transport mechanisms and overall dysfunctional biological activity, immune activation and inflammation. Nutritional stress, such as that caused by excess high-fat and/or carbohydrate diets, promotes oxidative stress as evident by increased lipid peroxidation products, protein carbonylation and decreased antioxidant status. In obesity, chronic oxidative stress and associated inflammation are the underlying factors that lead to the development of pathologies such as insulin resistance, dysregulated pathways of metabolism, diabetes and cardiovascular disease through impaired signalling and metabolism resulting in dysfunction to insulin secretion, insulin action and immune responses. However, exercise may counter excessive levels of oxidative stress and thus improve metabolic and inflammatory outcomes. In the present article, we review the cellular and molecular origins and significance of ROS production, the molecular targets and responses describing how oxidative stress affects cell function including mechanisms of insulin secretion and action, from the point of view of possible application of novel diabetic therapies based on redox regulation.

Aflatoxins are a class of carcinogenic mycotoxins produced by Aspergillus fungi and are known to contaminate a large portion of the world's food supply. Aflatoxin B1 (AFB1) is the most potent of these compounds and has been well-characterized to lead to the development of hepatocellular carcinoma (HCC) in humans and animals. This review focuses on the metabolism of AFB1, including epoxidation and DNA adduction, as it concerns the initiation of cancer and the underlying mechanisms. The link between AFB1 consumption and HCC is also discussed including synergistic interactions with the hepatitis B virus. Toxic effects of AFB1, including growth suppression, malnutrition, and immunomodulation, are also covered. This review also describes recent reports of AFB1 occurrence in global food supplies and exposures in occupational settings. Furthermore, a summary of recent detoxification methods is included to indicate the present state of the field in developing aflatoxin control methods. This information shows that AFB1 occurs frequently in food supplies at high concentrations, particularly in maize. Regarding detoxification methods, chemical control methods were the fastest methods that still retained high detoxification efficacy. The information presented here highlights the need to implement new and/or existing detoxification methods to reduce the global burden of AFB1 toxicity.