Transcriptional Changes after Enniatins A, A1, B and B1 Ingestion in Rat Stomach, Liver, Kidney and Lower Intestine

Abstract

Enniatins (ENs) are depsipeptide mycotoxins produced by Fusarium fungi. They are known for their capacity to modulate cell membrane permeability and disruption of ionic gradients, affecting cell homeostasis and initiating oxidative stress mechanisms. The effect of the acute toxicity of ENs A, A1, B and B1 at two different concentrations after 8 h of exposure was analysed in Wistar rats by a transcriptional approach. The following key mitochondrial and nuclear codified genes related to the electron transport chain were considered for gene expression analysis in stomach, liver, kidney and lower intestine by quantitative Real-Time PCR: mitochondrially encoded NADH dehydrogenase 1 (MT-ND1), mitochondrially encoded cytochrome c oxidase 1 (MT-COX1), succinate dehydrogenase flavoprotein subunit A and ATP synthase F1 subunit alpha, respectively. Moreover, the expression of markers involved in oxidative stresssuperoxide dismutase 1 (SOD1), glutathione peroxidase 1 (Gpx1), heme oxygenase 1, apoptosis B-cell lymphoma 2, Bcl2 Associated protein X (Bax), tumor suppressor protein (p53), inhibition of apoptosis nuclear factor kappa of activated B cells, immune system interleukin 1β and intestinal tight junction Occludin merely in lower intestine tissues have been investigated. For mitochondrial genes, the main differences were observed for MT-ND1 and MT-COX1, showing its deficiency in all selected organs. With regard to the intestinal barrier’s cellular response to oxidative stress, the activity of the antioxidant gene SOD1 was decreased in a dose-dependent manner. Similarly, the catalytic enzyme GPx1 was also downregulated though merely at medium dose employed. On the contrary, the pro-apoptotic Bax and p53 regulators were activated after ENs exposure, reporting a significant increase in their expression. Furthermore, the alteration of intestinal permeability was assessed by the abnormal activity of the tight junction protein occludin. In summary, ENs may generate mitochondrial disorders and induce oxidative stress in intestinal barrier function.

Pilot Study: Does Contamination with Enniatin B and Beauvericin Affect the Antioxidant Capacity of Cereals Commonly Used in Animal Feeding?

“…The negative influence of ENN B contamination was not observed in corn and barley flours, in which this value was significantly higher ( p < 0.05; Figure 2 ). The involvement of ENs mycotoxins in initiating oxidative stress mechanisms has been demonstrated in a recent study conducted on Wistar rats, in which the exposure to concentrations of ENs A, A1, B, and B1 decreased the activity of the antioxidant enzyme superoxide dismutase 1 as a consequence of oxidative stress [ 41 ]. We speculate that this effect could be transposed to a different matrix, wheat in our case, although the extrapolation of in vitro data to our context is not straightforward and should hence be performed with caution.…”

Coping with extremes: the Rumen Transcriptome and Microbiome Co-regulate Plateau Adaptability of Xizang Goat

“…Thus, a shared function of the Selenomonas and SLC26A9 genes in safeguarding the rumen of Xizang goats is theorized. Butyrivibrio, which is expressed in the majority of tissues, including blood vessels, the stomach, and platelets, and which is involved in platelet aggregation, vasodilation and contraction, and the regulation of gastric mucosal blood ow to maintain the stability of physiological functions of cells, tissues, and organs [49,50], was found to have a signi cant positive correlation with the highly expressed COX1 gene [51]. Additionally, the rumen Butyrivibrio is an important degrader and user of lignocellulosic plant materials.…”

Ethylcoprostanol modulates colorectal cancer cell proliferation and mitigates cytotoxicity of cholesterol metabolites in non-tumor colon cells

“…The efficiency values were in accordance with those previously described. 24 The sequence of the target and reference gene primers as well as the amplification efficiency are shown in the ESI. † 2.8.3 Retrotranscription.…”