Hassan Malekinejad; Johanna Fink-Gremmels
Volume 11, Issue 2 , June 2020, , Pages 97-103
Abstract
Molds and mycotoxins are contaminants of animal feed causing spoilage and clinical intoxication. Animal exposure to mycotoxins reflects diet composition with major differences occurring between animals kept predominantly of pastures, i.e. ruminants and horses, and those consuming formulated feed like ...
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Molds and mycotoxins are contaminants of animal feed causing spoilage and clinical intoxication. Animal exposure to mycotoxins reflects diet composition with major differences occurring between animals kept predominantly of pastures, i.e. ruminants and horses, and those consuming formulated feed like pigs and poultry. Mixed feeds are composed of several ingredients, often sourced from different continents. Subsequently, practitioners may confront endemic diseases and signs of toxin exposure related to toxins imported accidentally with contaminated feed materials from other countries and continents. Mycotoxins comprise more than 300 to 400 different chemicals causing a variety of clinical symptoms. Mycotoxin exposure causes major economic losses due to reduced performance, impaired feed conversion and fertility, and increased susceptibility to environmental stress and infectious diseases. In acute cases, clinical symptoms following mycotoxin ingestion are often non-specific, hindering an immediate diagnosis. Furthermore, most mold species produce more than one toxin, and feed commodities are regularly contaminated with various mold species resulting in complex mixtures of toxins in formulated feeds. The effects of these different toxins may be additive, depending on the level and time of exposure, and the intensity of the clinical symptoms based on age, health, and nutritional status of the exposed animal(s). Threshold levels of toxicity are difficult to define and discrepancies between analytical data and clinical symptoms are common in daily practice. This review aims to provide an overview of Aspergillus and Penicillium toxins that are frequently found in feed commodities and discusses their effects on animal health and productivity.
Hassan Malekinejad; Nazli Alizadeh-Tabrizi; Araz Ostadi; Johanna Fink-Gremmels
Volume 6, Issue 1 , March 2015, , Pages 9-15
Abstract
The pathogenesis of equine grass sickness (EGS) has not fully understood. A better understanding of the exact pathogenesis of diseases can help to make an accurate diagnosis. Previous studies reported some pathological damage of neuronal cells in EGS patients. In this study, primarily cytotoxicity of ...
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The pathogenesis of equine grass sickness (EGS) has not fully understood. A better understanding of the exact pathogenesis of diseases can help to make an accurate diagnosis. Previous studies reported some pathological damage of neuronal cells in EGS patients. In this study, primarily cytotoxicity of serum from three clinically EGS-diagnosed horses on PC12 Tet-off (PTO) cells was assessed. Subsequently, the apoptotic tests including cytochrome C release, caspase-3/7 activity measurement and DNA fragmentation assay were conducted to clarify the apoptotic effect of serum from EGS patients. Addition of serum from EGS patients at concentrations higher than 25% on PTO cells resulted in a significant cytotoxicity in Alamar blue reduction assay compared with serum from healthy horses. All three apoptotic endpoints showed that the serum from EGS patients does have capability to induce apoptosis. A remarkable up regulation of cytochrome C release accompanied with concentration- and time-dependent augmentation in caspase-3/7 activity and ultimately DNA fragmentation were observed. Our data suggest that serum from EGS patients might have potentially neurotoxic compounds, which exerts cytotoxic and apoptotic effects on neuronal cells. Moreover, the EGS serum-induced apoptosis attributes to augmentation of cytochrome C release and caspase-3/7 activity.
