ORIGINAL RESEARCH
Mitigation of Organ Specific Toxicity Following
Acute Dinotefuran Exposure through
Vitamin C Supplementation
			
	
 
More details
Hide details
	
	
									
				1
				Institute of Biochemistry and Biotechnology, University of Veterinary and Animal Sciences, Lahore, Pakistan
				 
			 
						
				2
				Hameed Latif teaching Hospital, Lahore, Pakistan
				 
			 
						
				3
				Institute of Pharmaceutical Sciences, University of Veterinary and Animal Sciences, Lahore, Pakistan
				 
			 
										
				
				
		
		 
			
			
			
			 
			Submission date: 2023-09-11
			 
		 		
		
			
			 
			Final revision date: 2023-12-27
			 
		 		
		
		
			
			 
			Acceptance date: 2024-02-07
			 
		 		
		
			
			 
			Online publication date: 2024-04-11
			 
		 		
		
			
			 
			Publication date: 2024-07-12
			 
		 			
		 
	
							
																														    		
    			 
    			
    				    					Corresponding author
    					    				    				
    					Rahat  Naseer   
    					Institute of Biochemistry and Biotechnology, University of Veterinary and Animal Sciences, Lahore, Pakistan
    				
 
    			
				 
    			 
    		 		
			
							 
		
	 
		
 
 
Pol. J. Environ. Stud. 2024;33(5):5533-5540
		
 
 
KEYWORDS
TOPICS
ABSTRACT
The objective of this research was to assess the impact of 2-methyl-2-nitro-3-guanidine on
mammalian species, otherwise not the intended targets, followed by one-time exposure and its adverse
effects. Thirty-five Sprague Dawley rats of either male or female sex, aged four weeks, and with an
average weight of 80±20g, were divided into three groups randomly: control E exposed and exposed and
supplemented with vitamin C, and assigned the titles C,E, and V, respectively. Each group comprised
fifteen rats. Both E and V groups were further divided into subgroups: E1, E2, and E3, exposed to LD10,
LD25, and LD50 doses of Dinotefuran respectively, and V1, V2, and V3, exposed in the same manner
but supplemented with a fixed dose of ascorbic acid (vitamin C).
Ascorbic acid was administered in aqueous form 35mg/100mL of water and provided ad libitum.
Eight hours after exposure to Dinotefuran, 5ml of blood was collected under sedation through the
cardiac vein. After 48 hours, two rats randomly selected from each subgroup, including the control
group, were anesthetized, euthanized, and dissected. Different body tissues, and the kidney, liver,
bones, and heart, were isolated and preserved in formalin solution for subsequent analysis. CBC, liver,
renal, and cardiac biomarkers were evaluated. In addition, histopathology and bone characteristics
of soft tissues were also conducted. Mortality and morbidity were recorded.
The result showed significant disruptions in CBC and other biomarkers related to kidney, liver,
and heart in a dose-dependent pattern. Although vitamin supplementation improved the overall
outcome, the improvement was not statistically significant. Histopathological examination displayed
changes in the exposed (E) group, with no observable improvements with vitamin supplementation.
Moreover, the bone-related parameters exhibited similar trends.