Effect of Mycotoxins on Egg Quality01 March 2015
Giving hens mouldy feed supplemented with a mycotoxin inactivator, Toxy-Nil Plus, resulted in yolk carotenoid levels and plasma uric acid concentrations after 20 and 50 days of the experiment being similar to hens fed good feed and restored egg production, according to Nutriad.
Low levels of dietary mycotoxins are responsible for reduced efficiency of poultry production and increased susceptibility to infectious diseases. Inclusion of mycotoxin inactivators with complex matrix into poultry feeds might protect birds from some adverse effects of mycotoxins.
Mycotoxins in the diet of layers resulted in reduced carotenoid content in egg yolk and elevated plasma uric acid level. Inclusion of the mycotoxin inactivator, Toxy-Nil Plus, into mycotoxin-contaminated diet resulted in improved egg mass production and higher levels of carotenoids in egg yolk. Supplementation with the product was also able to reduce elevated plasma uric acid in birds fed mycotoxin-contaminated diet.
Mycotoxins are unavoidable contaminants in foods and feeds and are a serious problem all over the world. The number of mycotoxins known to cause signs of toxicity in mammals and birds is increasing. The most important mycotoxins in naturally contaminated foods and feeds are aflatoxins, ochratoxin A, zearalenone, T-2 toxin, deoxynivalenol (vomitoxin, DON) and fumonisins, and in many cases these mycotoxins can be found in combinations. Among all mycotoxins, those of Fusarium species are considered to be main contaminants of poultry feed.
Acute mycotoxicosis outbreaks are sporadic events in modern poultry production. Nevertheless, low or undetectable levels of mycotoxins are responsible for reduced performance and increased susceptibility to infectious diseases. The problem is even more complex since in many cases the molecular mechanisms of their action have not been fully explained.
Mycotoxins affect lipid metabolism
Biochemical changes during mycotoxicosis can vary significantly and lipid peroxidation is regarded as one of the key effects of mycotoxicosis. It is not clear whether mycotoxins stimulate lipid peroxidation directly by enhancing free radical production or if the increased tissue susceptibility to lipid peroxidation is a result of decreased antioxidant protection. It is likely that both processes are involved.
An effect of mycotoxins on lipid peroxidation in vivo has been reported by number of authors. Many mycotoxins are lipophilic substances and are readily absorbed into the membrane, resulting in structural alteration within the membranes. That triggers the stimulation of membranous lipid peroxidation. Ochratoxin A, T-2 toxin, fumonisins and aflatoxin were shown to have pro-oxidant properties. There are also data available indicating pro-oxidant properties of zearalenone and citrinin.
In most cases lipid peroxidation in tissues caused by mycotoxins was associated with decreased concentrations of natural antioxidants in blood serum, liver and ovary. For example, α-tocopherol, γ-tocopherol, carotenoids and ascorbic acid significantly decrease as a result of mycotoxins consumption.
A delicate balance between antioxidants and pro-oxidants in the body in general and specifically in the cell is responsible for regulation of various metabolic pathways. Nutritional stress factors have a negative impact on this antioxidant/pro-oxidant balance. In this respect, mycotoxins can be considered among the most important feed-borne stress factors.
Decreased intestinal absorption of fat-soluble nutrients when mycotoxins are present in feed
After ingestion carotenoids are absorbed in the small intestine together with other fat-soluble nutrients and delivered to the liver and then to the egg yolk. The efficiency of absorption and assimilation of carotenoids are known to be affected by components in the diet and general health of the hen.
Reduced adsorption (malabsorption) is a state arising from abnormality in absorption of food nutrients across the gastrointestinal (GI) tract. Malabsorption syndrome is characterised by stunted growth and a lack of skin pigmentation in poultry, most commonly broiler breeds. The disease has been identified in all countries with intensive poultry production. The problem appears to be multifactorial. In general, malabsorption syndrome is considered a common result of mycotoxicosis. Mycotoxins may act independently or interact with other factors such as genetics, hormonal status and age.
Mycotoxins cause decreased intestinal absorption of fat soluble nutrients, for example, they interfere with the absorption, transport and deposition of carotenoids. Mycotoxins stimulate lipid peroxidation in enterocytes leading to damage that could substantially contribute to malabsorption development.
Pale yolk of table eggs and bad quality of breeding eggs
Our preference for golden yellow egg yolks is rooted in history. Pale yolks were always a sign of sick hens, worm infestation or poor feed. Only healthy, well-nourished hens store carotenoids in their yolks. Bright golden-yellow yolks show that the hens are well supplied with essential carotenoids such as lutein or canthaxanthin. These protective substances are widely found in nature; they not only give the yolk its yellow colour but also prevent the oxidation and destruction of fragile, vital substances such as vitamins in the egg.
One of the most important targets for mycotoxins in breeders’ feed is embryonic development. Contamination of the diet with mycotoxins increase late mortality of embryos, increase the number of infertile eggs and impair hatchability. Since chicken embryo tissues contain high levels of polyunsaturated fatty acids (PUFA), they are vulnerable to peroxidation, and oxidative stress caused by mycotoxins could be lethal. Carotenoids are involved in regulation of embryonic development by way of their antioxidant properties.
Since lipid peroxidation plays an important role in mycotoxin toxicity, a protective effect of a complex mycotoxin inactivator is expected.
Layers fed a diet contaminated with T-2 toxin, deoxynivalenol, nivalenol and ochratoxin A had an impaired egg quality combined with the reduced egg production (Table 1).
|Table 1. Effect of mycotoxins and a mycotoxin inactivator on the performance, yolk carotenoid
content and plasma uric acid in laying hens at 47 to 54 weeks of age
|Uric acid (µmol/l)|
in yolk (µg/g)
|day 0||day 20||day 50|
|Control||18.3 a ±0.9||56.1 a ±3.9||325.6 a ±33.9||160.0 a ±10.0||170.4 a ±6.4|
|Mouldy feed *||15.6 b ±1.3||43.7 b ±4.2||360.3 a ±36.1||357.3 b ±34.9||368.9 b ±14.1|
|Mouldy feed + 2.5kg/tonne Toxy-Nil Plus||17.9 a ±1.1||49.9 ab ±2.8||333.9 a ±43.11||166.0 a ±15.8||148.3 a ±7.3|
|* 324mg/kg T-2 toxin; 218mg/kg deoxynivalenol; 87mg/kg nivalenol and 16mg/kg ochratoxin A
Values within rows with no common letters are significantly different (P<0.05)
The carotenoid content in yolk was significantly lower (15.5 versus 18.3mg per g) when mycotoxins were present in feed. Daily egg mass in the same group was 12.4g lower compared to the control group. The significantly increased plasma uric acid levels after 20 and 50 days of experiment in poultry hens fed mouldy feed confirmed the higher level of oxidative stress caused by the consumption of mycotoxins.
Giving birds bad quality feed supplemented with a mycotoxin inactivator with complex matrix resulted in yolk carotenoid levels and plasma uric acid concentrations after 20 and 50 days of the experiment being similar to hens fed good feed.
Inclusion of the protective additive, Toxy-Nil Plus, into feed showed the trend in improvement in egg mass production.