Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3122
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
We investigated the effects of N-acetyl cysteine (NAC) on transient receptor potential melastatin 2 (TRPM2) channel expression in rat kidney and liver tissues following experimental malathion intoxication. We used seven groups of six male Wistar albino rats: control group, NAC, pralidoxime + atropine, malathion, malathion + pralidoxime + atropine, malathion + pralidoxime + atropine + NAC, and malathion + NAC. Single doses of 100 mg/kg N-acetyl cysteine, 40 mg/kg pralidoxime, 2 mg/kg atropine and 1/3 the lethal dose of malathion were administered. No difference in malondialdehyde (MDA) levels, apoptosis or TRPM2 immunoreactivity was found in liver tissue among the groups. In kidney tissue, MDA levels, apoptosis and TRPM2 immunoreactivity were increased significantly in the malathion and malathion + NAC groups compared to the control group. We found that organophosphate intoxication did not affect MDA, apoptosis or TRPM2 immunoreactivity in rat liver during the acute period. By contrast, we found that in kidney tissue, MDA, apoptosis, and TRPM2 immunoreactivity were increased significantly following administration of malathion. Also, NAC given in addition to pralidoxime and atropine reduced MDA to control levels.
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Source |
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http://dx.doi.org/10.1080/10520295.2021.1986639 | DOI Listing |
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