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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their respective doses every other day for 9 weeks, followed by a 9-week recovery period where all drugs were withdrawn.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.

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Gonadotropin-releasing hormone (GnRH)–loaded chitosan nanoparticles (GnRH–ChNPs) were used at different doses and routes of administration to induce ovulation in rabbits as an attempt to improve artificial insemination (AI) procedures and outcomes. In this study, the characteristics (size, polydispersity, loading efficiency, and zeta-potential) of GnRH–ChNPs and the GnRH release pattern were determined in an in vitro study. A first in vivo study assessed the pituitary and ovarian response to different GnRH–ChNPs doses and routes of administration (two i.m. doses, Group HM = 0.4 µg and Group QM = 0.2 µg, and two intravaginal doses, Group HV = 4 µg and Group QV = 2 µg) against a control group (C) receiving bare GnRH (0.8 µg). The HM, QM, and HV treatments induced an earlier LH-surge (90 min) than that observed in group C (120 min), whilst the QV treatment failed to induce such LH surge. The number of ovulation points was similar among treatments, except for the QV treatment (no ovulation points). A second in vivo study was consequently developed to determine the hormonal (progesterone, P4, and estradiol, E2) profile and pregnancy outcomes of both HM and HV treatments against group C. The treatment HM, but not the treatment HV, showed adequate P4 and E2 concentrations, conception and parturition rates, litter size, litter weight, and viability rate at birth. Overall, the use of GnRH–ChNPs allows for a reduction in the conventional intramuscular GnRH dose to half without compromising fertility. However, the addition of GnRH–ChNPs to semen extenders, although successfully inducing ovulation, has negative impacts on fertility. Thus, more studies are needed to explore this point and allow further adjustments.

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