Influence of Ascorbic Acid Supplementation on the Haematological and Clinical Biochemistry Parameters of Male Rabbits Exposed to Aflatoxin B₁

Abstract

This study was undertaken to evaluate the effectiveness of L-ascorbic acid (AA) in alleviating the toxicity of aflatoxin B1 (AFB1) in male New-Zealand white rabbits. Five rabbits (6 months of age and mean body weight 3.12 kg) per group were assigned to 1 of 6 treatment groups: 0 mg AA and 0 mg AFB1/kg BW (control); 20 mg AA/kg BW; 15 microg AFB1/kg BW; 15 microg AFB1 plus 20 mg AA/kg BW; 30 pg AFB1/kg BW; 30 pg AFB1 plus 20 mg AA/kg BW. Rabbits were orally administered their respective doses every other day for 9 weeks, followed by a 9-week recovery period where all drugs were withdrawn. Evaluations were made for hemato-biochemical parameters and enzymatic activities. Results showed that AFB1 significantly (p< 0.05) decreased hemoglobin (Hb), total erythrocytic count (TEC) and packed cell volume (PCV), in a dose-dependent manner, and these effects were continued during the recovery period. Ascorbic acid caused an increase in these parameters, and alleviated the negative effect of AFB1 during the treatment period. Additionally, serum concentrations of total protein, albumin and glucose were significantly (P < 0.05) declined by treatment with the high dose of aflatoxin and these effects were continued during the recovery period. Ascorbic acid caused non-significant increases in these parameters and alleviated the harmful effect of AFB1. On the other hand, aflatoxin treatment caused significant increases (P < 0.05) in the activities of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (AlP) during the treatment period in a dose dependent manner, and this effect was continued during the recovery period, especially with the high dose. Also, treatment with the high dose of aflatoxin caused significant increases (P<0.05) in cholesterol and total bilirubin. Ascorbic acid caused significant decreases in these parameters and alleviated the harmful effects of AFB1. Whereas, Total leukocyte count (TLC), urea and creatinine were not significantly affected by aflatoxin-treatment. Generally, it is interesting feature that the treatment with AA alone had no negative effects on most of the previous parameters. Also, the presence of AA could diminished the adverse effects of AFB1 on most of hematological and biochemical values, and enzymatic activities in rabbits.

Assessment of a natural dietary extract, titrated in phenylpropanoid glycosides, on blood parameters and plasma oxidative status in intensively reared Italian hares (Lepus corsicanus)

“…Similarly, Yousef et al (2003) observed that rabbits fed a diet enriched with antioxidants, such as ascorbic acid, had lower bilirubin levels after daily ingestion of aflatoxin B1.…”

Protective effects of curcumin, vitamin C, or their combination on cadmium-induced hepatotoxicity

“…Vitamin C is an essential cofactor for many enzymes involved in diverse metabolic pathways [47]. Sahin et al [48] found that serum activities of SGOT and SGPT were not infl uenced by dietary vitamin C. Also, Yousef et al [49] and Yousef [50] found that rabbits treated with vitamin C did not show any changes in the activities of AST and ALT. Th is is in accordance with our results showing that vitamin C had no signifi cant eff ects in prevention against liver damages in Cd intoxicated rats.…”

Protective Effect of Black Tea Infusion on Aflatoxin-Induced Hepatotoxicity in Mice

“…It is known that liver is the pivotal organ which is responsible for the secretion of majority of serum proteins and decrease in protein biosynthesis and also reduced secretion due to the ability of aflatoxin to for abducts with DNA and RNA will decrease the concentration of serum proteins. Aflatoxins have previously been shown to lower the total protein concentration in serum of pigs, 35 rabbits 36 and broilers. 37 It is well known that leakage of hepatic housekeeping enzymes namely ALT (normal range in mice: 17-77 U/L) and AST (normal range in mice: 54-298 U/L) 38 serve as biochemical indices of hepatocellular damage and recovery offered by therapeutic agents indicates hepatoprotection.…”