Rafid Khalid Ali
Department of pathology, College of Veterinary Medicine, University of Fallujah, Iraq
Zahraa S. Mahdi
Healthy and Medical technical College, AL-Zahraa University for Women, Kerbalaa, Iraq
Ahmed Jasim Nawfal
Department of physiology and medical physics, College of Medicine, University of Fallujah, Iraq
ABSTRACT
Background: Lead is a well-studied toxic metal known for its harmful physiological effects, which depend on the duration and intensity of exposure. Its widespread presence in soil, water, and food makes it a significant public health concern. Given the limitations of conventional treatments, there is increasing interest in alternative therapies, including the use of Vitamin B1, to mitigate lead toxicity. This study aimed to evaluate the protective effects of Vitamin B1 against lead acetate-induced liver and kidney damage in rabbits. Methods: Twenty-eight local rabbits were randomly assigned to four groups and treated daily for eight weeks as follows: Group 1 (control) received distilled water; Group 2 (lead-only) received lead acetate (5 mg/kg BW); Group 3 received Vitamin B1 (75 mg/head) plus lead acetate (5 mg/kg BW); and Group 4 received Vitamin B1 (150 mg/head) plus lead acetate (5 mg/kg BW). Vitamin B1 was administered daily, while lead acetate was given every 48 hours. Blood samples were collected via cardiac puncture at weeks 1, 4, and 8 to measure liver enzyme levels (ALT and AST) and glutathione reductase. Histopathological changes in the liver and kidneys were also analyzed. Results: The AST and ALT enzyme levels showed no significant differences between groups at weeks 1 and 4. However, by week 8, Group 2 (lead-only) exhibited a significant increase in AST levels compared to Groups 1, 3, and 4 (P<0.05). Within-group comparisons revealed significant elevations in AST levels in Group 2 between weeks 1, 4, and 8, whereas no significant changes were observed in the other groups. Histopathological examination indicated marked liver and kidney damage in Group 2, which was notably attenuated in the Vitamin B1-treated groups. Conclusion: Vitamin B1 demonstrated a protective effect against lead acetate-induced liver and kidney damage in rabbits, as evidenced by improved enzyme levels and reduced histopathological changes. These findings suggest that Vitamin B1 could be a potential therapeutic agent for mitigating the toxic effects of lead exposure.
Keywords: Histopathological Changes, Liver Damage, Lead Acetate, Oxidative Stress, Thiamin.
