ABSTRACT
The impact of zinc oxide nanoparticles (ZnO-NPs) on the pathogenesis of coccidiosis in broiler chickens was tested. A total of 160 1-day-old broiler chicks (Ross 308) were randomly allocated into 4 groups (n = 40). Group 1: unchallenged, unmedicated; Group 2: challenged, unmedicated; Group 3: challenged, supplemented with diclazuril (1 ppm); Group 4: challenged, supplemented with ZnO-NPs (20 ppm). Mixed Eimeria species (E. maxima, E. acervulina, E. mivati, and E. tenella) of a commercial coccidial vaccine (FORTEGRA®) were used to perform the coccidial challenge by 15× of its vaccinal dose on the 14th day of age. Diclazuril and ZnO-NPs supplementation in Group 3 and 4, respectively, reduced the mortality rate due to coccidial challenge to 5.8% compared to 11.9% in Group 2. The growth performance was improved by ZnO-NPs in coccidiosis-infected group (p ≤ 0.05) compared to Group 2 and was comparable to that of Group 3 (p ≥ 0.05). The average oocyst count was lower in Groups 3 and 4 (7.8 × 103 and 14.3 × 103, respectively) than in Group 2 (67 × 103 oocysts). Group 3 had a decreased gross lesion score in duodenum and caecum (p ≤ 0.05) as well as jujenum and ileum (p ≥ 0.05) compared to Group 2; while the average lesion scores of all intestinal parts in Group 4 were significantly decreased (p ≤ 0.05). However, diclazuril was superior to ZnO-NPs in reducing caecal lesion score (p ≤ 0.05). Plasma carotenoids levels were increased by diclazuril (p ≥ 0.05) and ZnO-NPs (p ≤ 0.05) supplementation compared to Group 2. Oxidative stress appeared on the fourth week post-challenge (pc) in Group 2 (p ≤ 0.05) compared to Group 1, while the dietary supplementation with either diclazuril or ZnO-NPs numerically decreased Malondialdhyde (p ≥ 0.05) and statistically increased antioxidant activity (p ≤ 0.05). Both medications significantly improved the PCV%, Hb% and RBCs count on the 6th-day and 4th-week pc (p ≤ 0.05) compared to Group 2, though this improvement was higher significantly in Group 4 than Group 3 on the 6th day pc (p ≤ 0.05). Neither coccidial challenge nor medications had an impact on the total WBCs count as well as organ index, except Bursa of fabricious index that significantly improved by ZnO-NPs on the 4th-week pc compared to Group 2. Coccidial challenge reduced total protein and globulin levels and increased the serum alanine aminotransferase, serum cholesterol, and low-density lipoprotein levels (p ≤ 0.05) compared to Group 1, while those of both medicated groups (Group 3 and 4) were comparable to Group 1 (p ≥ 0.05). In conclusion, ZnO-NPs were found to be as effective as diclazuril against coccidiosis. However, further research is needed to fully comprehend its anticoccidial mechanisms.
ABSTRACT
The present study aims to investigate the protective effects of zinc oxide nanoparticles (ZnO NPs) on doxorubicin-induced testicular injury. Forty mature male rats were randomly allocated into four equal groups: G1 (control), G2 (3 mg per kg BW of zinc oxide nanoparticles was administered), G3 (6 mg per kg BW of doxorubicin was intraperitoneally injected), and G4 (doxorubicin + ZnO NPs). Some fertility parameters, antioxidant status, genotoxicity assay, and a histopathological examination were used for this investigation. The doxorubicin-treated group showed a significant decrease in the index weight of reproductive organs, epididymal sperm count, motility%, and live sperm% and a significant increase in sperm abnormalities. Moreover, GSH and CAT activities were significantly decreased, and MDA content was significantly increased in the doxorubicin-treated group. Interestingly, co-administration of ZnO NPs significantly reduced the doxorubicin-induced changes in the investigated parameters. In addition, ZnO NPs alone did not show any undesirable effects on the sperm parameters, testis or DNA. However, its administration improves the reproductive parameters and significantly increases the testosterone level. We concluded that the administration of ZnO NPs at 3 mg per kg BW ameliorated the testicular toxicity and genotoxicity caused by doxorubicin through its antioxidant and androgenic activity.
