Effect of pH on the Mycelial Growth of Aspergillus niger and Aspergillus flavus

Aspergillus fungus is well-known for causing a number of secondary plant and food rots that can result in the buildup of mycotoxins, despite their significant economic contribution to the fermentation industries. In the past, even the most fundamental influences on the development and inhibition of significant mycotoxigenic fungi were only partially understood. To overcome this issue, an investigation on the impact of pH on the mycelial development of Aspergillus species was conducted. A. niger and A. flavus were inoculated in PDA medium with a range of pH values from 4.0 to 9.0 under in vitro conditions and then cultured for 7 days at room temperature. Results revealed that, the mycelial growth of A. niger and A. flavus was increased with increase in pH level up to 6 and then became static up to pH level 9 and there was no mycelial growth in pH 4. Hence, it was concluded that the use of alkaline compounds as a way of preventing their proliferation and reproductive processes may be used to inhibit the development and spore production of A. niger and A. flavus, which can affect the crops

Gut microbial degradation of organophosphate insecticides-induces glucose intolerance via gluconeogenesis

International audienceBACKGROUND:Organophosphates are the most frequently and largely applied insecticide in the world due to their biodegradable nature. Gut microbes were shown to degrade organophosphates and cause intestinal dysfunction. The diabetogenic nature of organophosphates was recently reported but the underlying molecular mechanism is unclear. We aimed to understand the role of gut microbiota in organophosphate-induced hyperglycemia and to unravel the molecular mechanism behind this process.RESULTS:Here we demonstrate a high prevalence of diabetes among people directly exposed to organophosphates in rural India (n = 3080). Correlation and linear regression analysis reveal a strong association between plasma organophosphate residues and HbA1c but no association with acetylcholine esterase was noticed. Chronic treatment of mice with organophosphate for 180 days confirms the induction of glucose intolerance with no significant change in acetylcholine esterase. Further fecal transplantation and culture transplantation experiments confirm the involvement of gut microbiota in organophosphate-induced glucose intolerance. Intestinal metatranscriptomic and host metabolomic analyses reveal that gut microbial organophosphate degradation produces short chain fatty acids like acetic acid, which induces gluconeogenesis and thereby accounts for glucose intolerance. Plasma organophosphate residues are positively correlated with fecal esterase activity and acetate level of human diabetes.CONCLUSION:Collectively, our results implicate gluconeogenesis as the key mechanism behind organophosphate-induced hyperglycemia, mediated by the organophosphate-degrading potential of gut microbiota. This study reveals the gut microbiome-mediated diabetogenic nature of organophosphates and hence that the usage of these insecticides should be reconsidered