Toxico-Pathological Effects of In Ovo Inoculation of Ochratoxin A (OTA) in Chick Embryos and Subsequently in Hatched Chicks

Abstract

This study was designed to investigate the toxico-pathological effects of in ovo inoculation of ochratoxin A (OTA) in chicken embryos and subsequently in the hatching chicks. Nine hundred fertile white leghorn (WL) layer breeder eggs were divided into eight groups (A-H). Group A was maintained as untreated control, whereas group B was kept as sham control (10 mL of 0.1 M NaHCO 3 solution). Before incubation, groups C, D, E, F, G, and H were injected with 0.01, 0.03, 0.05, 0.10, 0.50, and 1.00 mg OTA/egg, respectively. At 53 hrs of incubation, crown to rump length, optic cups, and eye lens diameters were significantly (p .05) lower, whereas neural tube closure defects were higher in the OTA-treated embryos. Teratogenic defects (studied at day 9 of incubation) and embryonic mortalities were higher in the groups administered high doses of OTA. A significant increase was noted in the serum concentration of ALT, urea, and creatinine, along with higher weights of liver and kidney, in chicks hatched from OTA-contaminated eggs. These findings suggested that there are teratogenic and substantive toxicological risks in the developing chicken embryos and hatched chicks that could be exposed to OTA in ovo.

Oxidative Stress of in-Ovo Ochratoxin A Administered during Chick Embryonic Development

“…Therefore, the increase in the allantoic fluid uric acid and creatinine levels may be due to a decrease in the glomerular filtration rate. The increase in the urea and creatinine levels may be due to nephrotoxic effects following the in-ovo inoculation of OTA (Zahoor-ul-Hassan et al, 2012).…”

“…The most relevant toxic effect of OTA in animal cells is the production of reactive oxygen species (ROS) that leads to the inhibition of protein synthesis; lipid peroxidation and DNA damage, all resulting in OTAmediated oxidative damage (Ringot et al, 2006). Evidence for a role of oxidative damage in the toxicological mutagenic, teratogenic, embryotoxic, hepatotoxic, and nephrotoxic properties of OTA has been collected and described (Zahoor-ul-Hassan et al, 2012). Antioxidants can counteract the deleterious effects of chronic consumption or exposure to OTA confirming the link between OTA toxicity and oxidative stress (Sorrenti et al, 2013).…”

Effects of three Bacillus specious on hatchability, growth performance and serum biochemistry in Japanese quails fed diet contaminated with Aflatoxin B1

“…It was reported that the adverse effects of AFB1 on embryo appeared in early life embryonic (Hassan et al, 2012). In many cases, researchers indicated that tetratogenic characteristics of mycotoxins could reduce hatchability by causing mandibular hypoplasia, softness and abnormality of the maxillary bone which impaired the final development of embryo (Hassan et al, 2012). One research demonstrated that breeder quails fed 4-6 ppb AFB have shown markedly decreased hatchability after 3 weeks (Howarth & Wyatt, 1976).…”

Toxicopathological and Serum Biochemical Alterations Induced by Ochratoxin a in Broiler Chicks and Their Amelioration by Locally Available Bentonite Clay

“…Ochratoxin, particularly OTA is considered as a potent carcinogen and classified in Group 2B by the International Agency for Research on Cancer (IARC, 1993) for humans. Ochratoxins are considered to be the main reason for causing a serious anomaly namely Balkan Endemic Nephropathy (BEN) in humans exposed to its dietary exposure (Zahoor-ul-Hassan et al, 2012;Solcan et al, 2015;Iftikhar et al, 2015;Ben Salah-Abbes et al, 2015). Ochratoxin A (OTA) causes adverse effects in poultry and is considered to be the most toxic mycotoxin along with aflatoxins for poultry birds.…”