Abstract
ABSTRACT The present work was carried out to study the effect of in-ovo injection of ochratoxin A (OTA) as an oxidative stress and its consequences on hepatic and kidney functions, thyroid activity, and histological examination of brain and liver in chicken embryos and subsequently in the hatching chicks. On the 10th day of incubation, one hundred and sixty-two fertile eggs were randomly divided into two equal treatments. Control treatment, (injected by 50 µl sodium carbonate) and OTA treatment (injected by 12.5 ng OTA dissolved in 50 µl sodium carbonate). OTA treatement group significantly reduced glutathione (GSH) and significantly increased thiobarbituric acid reactive substances production (TBARS) in embryonic and hatched chicks regarding livers, spleen, bursa of Fabricius, heart, and brain as an indicator of oxidative stress. OTA injection increased TBARS and decreased GSH levels in both allantoic and amniotic fluids. On the 14th and 16th days of incubation and at the hatch, a significant lower concentration in cholesterol and higher concentrations of alanine amino transferase, aspartate amino transferase, alkaline phosphatase, gamma glutamyl transferase, acid phosphatase enzymes activities and triglycerides in the hepatic tissues of the OTA group were observed. Histological examination of OTA group of brain and liver tissues showed some degenerative changes through the experimental period. In conclusion, in-ovo OTA treated had teratogenic and embryotoxic effects.
Highlights
Ochratoxins are a group of structurally related, secondary metabolites produced by several toxigenic species of Aspergillus and Penicillium; they contaminate various raw agricultural commodities and have very diversified toxic effects in humans and animals (Battacone et al, 2010).The most relevant toxic effect of ochratoxin A (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)
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)
The effect of OTA as an oxidative stress was demonstrated by measuring thiobarbituric acid reactive substances (TBARS) and GSH levels in the brain, liver, spleen, bursa of Fabricius and heart of embryos and hatchlings
Summary
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). 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). OTA within a wide range of contamination (130 ug - 3.9 mg OTA/Kg) in poultry diets lead to the reduction in growth rate, feed consumption, feed efficiency, reduced immunity and increased mortality (Elaroussi et al, 2006). Chickens that consume sublethal doses of OTA lead to accumulate the toxin in their tissues and eggs, a dose response relationship was observed (Elaroussi et al, 2008). OTA was observed in all body tissues with the highest level in the kidney eRBCA-2019-0637
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