The co-occurrence and accumulation of mycotoxin in food and feed constitutes a major issue to food safety, food security, and public health. Accurate and sensitive mycotoxins analysis can avoid toxin contamination as well as reduce food wastage caused by false positive results. This mini review focuses on the recent advance in detection methods for multiple mycotoxins, which mainly depends on immunoassay technologies. Advance immunoassay technologies integrated in mycotoxin analysis enable simultaneous detection of multiple mycotoxins and enhance the outcomes' quality. It highlights toxicogenomic as novel approach for hazard assessment by utilizing computational methods to map molecular events and biological processes. Indeed, toxicogenomic is a powerful tool to understand health effects from mycotoxin exposure as it offers insight on the mechanisms by which mycotoxins exposures cause diseases.
Probiotic Lactobacillus casei Shirota (LcS) is a potential decontaminating agent of aflatoxin B1 (AFB1). However, few studies have investigated the influence of diet, especially a high protein (HP) diet, on the binding of AFB1 by probiotics. This research was conducted to determine the effect of HP diet on the ability of LcS to bind AFB1 and reduce aflatoxin M1 (AFM1) in AFB1-induced rats. Sprague Dawley rats were randomly divided into three groups: A (HP only), B (HP + 108 CFU LcS + 25 μg AFB1/kg BW), and C (HP + 25 μg AFB1/kg BW). Levels of AST and ALP were higher in all groups but other liver function's biomarkers were in the normal range, and the liver's histology showed no structural changes. The urea level of rats in group B (10.02 ± 0.73 mmol/l) was significantly lower (p < 0.05) than that of rats in group A (10.82 ± 0.26 mmol/l). The presence of carcinoma in the small intestine and colon was more obvious in group C than in group B. Moreover, rats in group B had significantly (p < 0.05) lower AFM1 concentration (0.39 ± 0.01 ng/ml) than rats in group C (5.22 ± 0.28 ng/ml). Through these findings, LcS supplementation with HP diet alleviated the adverse effects of AFB1 by preventing AFB1 absorption in the small intestine and reducing urinary AFM1.
The secondary metabolites produced by fungi known as mycotoxins, are capable of causing mycotoxicosis (diseases and death) in human and animals. Contamination of feedstuffs as well as food commodities by fungi occurs frequently in a natural manner and is accompanied by the presence of mycotoxins. The occurrence of mycotoxins' contamination is further stimulated by the on-going global warming as reflected in some findings. This review comprehensively discussed the role of mycotoxins (trichothecenes, zearalenone, fumonisins, ochratoxins, and aflatoxins) toward gut health and gut microbiota. Certainly, mycotoxins cause perturbation in the gut, particularly in the intestinal epithelial. Recent insights have generated an entirely new perspective where there is a bi-directional relationship exists between mycotoxins and gut microbiota, thus suggesting that our gut microbiota might be involved in the development of mycotoxicosis. The bacteria-xenobiotic interplay for the host is highlighted in this review article. It is now well established that a healthy gut microbiota is largely responsible for the overall health of the host. Findings revealed that the gut microbiota is capable of eliminating mycotoxin from the host naturally, provided that the host is healthy with a balance gut microbiota. Moreover, mycotoxins have been demonstrated for modulation of gut microbiota composition, and such alteration in gut microbiota can be observed up to species level in some of the studies. Most, if not all, of the reported effects of mycotoxins, are negative in terms of intestinal health, where beneficial bacteria are eliminated accompanied by an increase of the gut pathogen. The interactions between gut microbiota and mycotoxins have a significant role in the development of mycotoxicosis, particularly hepatocellular carcinoma. Such knowledge potentially drives the development of novel and innovative strategies for the prevention and therapy of mycotoxin contamination and mycotoxicosis.
There are different types of nutritionally mediated oxidative stress sources that trigger inflammation. Much information indicates that high intakes of macronutrients can promote oxidative stress and subsequently contribute to inflammation via nuclear factor-kappa B- (NF-κB-) mediated cell signaling pathways. Dietary carbohydrates, animal-based proteins, and fats are important to highlight here because they may contribute to the long-term consequences of nutritionally mediated inflammation. Oxidative stress is a central player of metabolic ailments associated with high-carbohydrate and animal-based protein diets and excessive fat consumption. Obesity has become an epidemic and represents the major risk factor for several chronic diseases, including diabetes, cardiovascular disease (CVD), and cancer. However, the molecular mechanisms of nutritionally mediated oxidative stress are complex and poorly understood. Therefore, this review aimed to explore how dietary choices exacerbate or dampen the oxidative stress and inflammation. We also discussed the implications of oxidative stress in the adipocyte and glucose metabolism and obesity-associated noncommunicable diseases (NCDs). Taken together, a better understanding of the role of oxidative stress in obesity and the development of obesity-related NCDs would provide a useful approach. This is because oxidative stress can be mediated by both extrinsic and intrinsic factors, hence providing a plausible means for the prevention of metabolic disorders.
Aging is the progressive loss of organ and tissue function over time. Growing older is positively linked to cognitive and biological degeneration such as physical frailty, psychological impairment, and cognitive decline. Oxidative stress is considered as an imbalance between pro- and antioxidant species, which results in molecular and cellular damage. Oxidative stress plays a crucial role in the development of age-related diseases. Emerging research evidence has suggested that antioxidant can control the autoxidation by interrupting the propagation of free radicals or by inhibiting the formation of free radicals and subsequently reduce oxidative stress, improve immune function, and increase healthy longevity. Indeed, oxidation damage is highly dependent on the inherited or acquired defects in enzymes involved in the redox-mediated signaling pathways. Therefore, the role of molecules with antioxidant activity that promote healthy aging and counteract oxidative stress is worth to discuss further. Of particular interest in this article, we highlighted the molecular mechanisms of antioxidants involved in the prevention of age-related diseases. Taken together, a better understanding of the role of antioxidants involved in redox modulation of inflammation would provide a useful approach for potential interventions, and subsequently promoting healthy longevity.
Oil palm empty fruit bunch (EFB) is the most significant waste generated from the agricultural industry in Malaysia. Composting is one of the potential approaches to utilize EFB. However, composting of EFB is a time-consuming process, thus impractical for industrial application. The composting process can be shortened by introducing competent fungi into an optimal EFB composting system. This study was conducted to isolate and identify competent fungi that can naturally compost EFB. Samplings were carried out at eight different time points over a 20-weeks experimental period. The physical properties of EFB samples such as pH, residual oil content, and moisture content were measured and the EFB composting process that was indicated by the contents of cellulose, hemicellulose, and lignin were assessed. The fungal growth, distribution, and lignocellulolytic enzyme activities were evaluated. The results indicated that the changes in physical properties of EFB were correlated to the fungal growth. The gradual reduction in moisture content and residual oil, and the increment in pH values in EFB samples throughout the experimental period resulted in reduced fungal growth and diversity. Such phenomenon delayed EFB composting process as revealed by the changes in EFB lignin, hemicellulose, and cellulose contents. The most dominant and resilient fungi (Lichtheimia ramosa and Neurospora crassa) survived up to 16 weeks and were capable of producing various lignocellulolytic enzymes. Further understanding of these factors that would contribute to effective EFB composting could be useful for future industrial applications.
The use of probiotic as dietary approach to prevent exposure to food contaminant, aflatoxin B1 (AFB1) has greatly increased. Several studies found that AFB1 binding to the bacterial cell wall is strain-specific. Moreover, the interaction between AFB1 and bacterial cell wall is not well-understood, thus warrants further investigation. This research was conducted to assess the ability of Lactobacillus casei Shirota (Lcs) to bind AFB1 at different concentrations and to determine AFB1 binding efficiency of different Lcs cell components including live cell, heat-treated, and cell wall. In addition, the interaction between AFB1 and Lcs was also evaluated via scanning electron microscopy (SEM) and through an animal study. The binding of AFB1 by all Lcs cell components depends on the concentration of available AFB1. Among all Lcs cell components, the live Lcs cells exhibited the highest binding efficiency (98%) toward AFB1. Besides, the SEM micrographs showed that AFB1 induced structural changes on the bacterial cell surface and morphology including rough and irregular surface along with a curve rod-shaped. In vivo experiment revealed that Lcs is capable to neutralize the toxicity of AFB1 on body weight and intestine through the binding process. The animal's growth was stunted due to AFB1 exposure, however, such effect was significantly (p < 0.05) alleviated by Lcs. This phenomenon can be explained by a significant (p < 0.05) decreased level of blood serum AFB1 by Lcs (49.6 ± 8.05 ng/mL) compared to AFB1-exposed rats without treatment (88.12 ± 10.65 ng/mL). Taken together, this study highlights the potential use of Lcs as a preventive agent against aflatoxicosis via its strong binding capability.
The modulation of gut microbiota and proteome due to aflatoxin B1 (AFB1) by probiotics remains unclear. This study investigated the alterations of gut microbiota and proteome in AFB1-exposed rats treated with probiotic Lactobacillus casei Shirota (Lcs). Forty male Sprague Dawley rats were randomly divided into five groups (n = 8) comprised control, AFB1, AFB1+activated charcoal, AFB1+Lcs, and Lcs groups. The rats were subjected to different treatments via oral gavage for four weeks. Urine and serum were collected for the measurement of AFB1 biomarkers and organs were harvested for histological analysis. Metagenomic sequencing was performed on fecal samples to profile gut microbiota. Besides, AFB1 most affected organ i.e. jejunum was subjected to proteomic analysis. The results indicated that Lcs intervention significantly reduced AFB1 biomarkers. H&E-stained intestine showed Lcs alleviated AFB1-induced inflammation and abnormal cell growth, particularly at the jejunum. Although AFB1 increased potentially pathogenic bacteria and reduced beneficial bacteria abundance in feces, the microbiota composition was normalized with Lcs treatment. The gut proteome analysis of the jejunum sample showed several pathways of AFB1 toxicity, wherein Lcs treatment demonstrated its protective effect. It is concluded that metagenomic and proteomic approaches are useful tools to understand AFB1-Lcs interaction and detoxification mechanism in the gut.