Effects Of Curcumın, Sulforaphane And Intralıpıd İn The Management Of Organophosphate Toxİcİty
Organophosphate Intoxication Treatment
DOI:
https://doi.org/10.5281/zenodo.5776464Keywords:
Organophosphate poisoning, Curcumin, Sulforaphane, intralipidAbstract
Organophosphates are a group of chemical agents with frequent exposure due to accidents, suicide attempts or occupational reasons consisting of agricultural and industrial usage (1). The aim of the present study is to examine the influence of curcumin, sulforaphane and intralipid treatments with known antioxidant effects in organophosphate poisoning.
In the experimental study, an organophosphate toxicity model was created by administering a dose of 30 mg / kg p.o malathion (MAL) to 30 rats divided into five equal groups, excluding the control group. Electrocardiography (ECG) and electromyography (EMG) examinations were performed on all rats at the 2nd and 12th hours and curcumin, sulforaphane and intralipid were administered in certain doses to rats other than the control group. In the liver and kidney tissue samples taken after the rats were sacrificed at the 24th hour; Superoxide Dismutase (SOD), Active Glutathione (GSH), Malondialdehyde (MDA) levels were assessed, whereas in the serum; Alanine aminotransferase (ALT), Aspartate transaminase (AST), urea, creatinine and pseudocholinesterase levels were studied.
The pseudocholinesterase (PChE) levels of the rats were significantly lower in the organophosphate group, and ALT and AST levels were significantly higher. There was no significant difference in the levels of SOD, MDA and GSH. Electrocardiography (ECG) and electromyography (EMG) results were evaluated as normal in all groups.
In the present study, it is thought that curcumin may have a therapeutic effect on liver tissues in organophosphate toxicity, while sulforaphane and intralipid may be effective in liver tissues by showing antioxidant properties and reducing organophosphate-induced pseudocholinesterease suppression, respectively. Additionally, it is suggested that ECG and EMG alone are not sufficient in evaluating cardiotoxicity and neurotoxicity in the acute period.
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