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
Objective: To investigated the relationship between skin-tumor promotion and oxidative stress caused by dimethylated arsenic in mice.
Methods: The experimental animal model was used to examine the effect of dimethylated arsenic, a metabolite of DMA(V), dimethylarsinous acid (DMA(III)) in skin tumorigenesis in mice. The 8-oxo-2'-deoxyguanosine (8-oxodG) analysis of epidermis was based on the method of HPLC.
Results: When mice were topically treated with trivalent dimethylated arsenic (DMA(III)), a further reductive metabolite of DMA(V), not only an increase in skin tumors but also an elevation of 8-oxodG in epidermis were observed.
Conclusion: These results suggest that tumor promotion due to DMA(V) administration is mediated by DMA(III) through the induction of oxidative stress.
Download full-text PDF |
Source |
---|
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!