Severity: Warning
Message: file_get_contents(https://...@gmail.com&api_key=61f08fa0b96a73de8c900d749fcb997acc09&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 197
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 197
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 271
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3165
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 597
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 511
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 317
Function: require_once
98%
921
2 minutes
20
Pyrrolnitrin, a natural antifungal compound from sp. O33 was compared with the phenylpyrrole fungicides fludioxonil and fenpiclonil through metabolomic analysis of . Phenylpyrrole fungicides are traditionally known to disrupt the high-osmolarity glycerol (HOG) pathway. However, recent studies suggest additional mechanisms for fludioxonil, including reactive oxygen species (ROS) generation and mitochondrial dysfunction. ROS generation and membrane permeability assays showed that pyrrolnitrin induced the highest ROS accumulations, while phenylpyrrole fungicides induced both ROS production and increased membrane permeability. Metabolomic analysis revealed that pyrrolnitrin and phenylpyrrole fungicides inhibit key metabolic pathways, including the TCA cycle, amino acid metabolism, and nucleic acid metabolism, with consistent metabolite changes across these pathways. This study identifies mitochondrial dysfunction and metabolic disruption as shared mechanisms of pyrrolnitrin and phenylpyrrole fungicides.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1021/acs.jafc.5c01826 | DOI Listing |