Effects of ochratoxin A on membrane phospholipids of the intestine of broiler chickens, practical consequences

Abstract

Ochratoxin A (OTA) is a mycotoxin produced by various species of Aspergillus and Penicillium. Ochratoxin A was classified as a group 2B carcinogen and is one of the major intestinal pathogenic mycotoxins. One of the most frequent modes of intoxication is consumption of contaminated food with mycotoxins. Feed represents the major cost and has a direct impact on the economical viability of broiler’s production system, since it must contain the necessary elements that allow the animal to express the maximum genetic potential while providing its nutritional requirements. Thus, the animal has to digest the feed and absorb its nutrients, which is in direct correlation with the gastrointestinal tract, especially the small intestine and the development of the mucosal surface area. Once ingested, OTA is absorbed by passive diffusion, mainly the jejunum. Ochratoxin A’s presence affects lipid membranes and could lead to the degradation of their normal structure and functionality. All of these effects contribute to the development of malabsorption. It was very interesting to study the effect of OTA on the layer of phospholipids of the bowel. The experimental group received OTA (0.05 to mg/kg BW) through an intra-peritoneal injection, every other day for 21 days. We noted that feed conversion ratio and average daily gain were reduced. Histological studies showed important alterations at the level of the mucosal membrane of the intestine (villosities, crypts) following intra-peritoneal administration of the mycotoxin. Thinning and enlargement at the base of the villosities, hyperplasia and crypts in irregular forms, blunting and denudation were observed through the examination of intestinal morphology. Biochemical studies, such as total lipid and phospholipid compositions, allowed us to have more detailed results. All identified mucosal phospholipids were modified, particularly the phosphatidylcholine (PC) and the phosphatidylethanolamine (PE) in the jejunum mucosa. In fact, there was a decrease by 55.81% for PC, 56.66% for PE, while a significant increase by 32.91% was noted for phosphatidylserine in the jejunum. It was very interesting to study the effect of OTA on the phospholipids layer of the bowel, as the mucous membrane of the small intestine represents the main site of absorption and transformation of nutriments. To avoid such disturbances and prevent the effects of the OTA, precautions must be taken to inhibit mold growth at the level of the feed manufactory units. Phosphatidylcholine and PE administrations may represent an option that could allow reestablishment of phospholipid equilibrium in the intestine.

Dramatic shifts in intestinal fungal community between wintering Hooded Crane and Domestic Goose

“…Furthermore, we found two genera with high relative abundance (i.e., Aspergillus and Talaromyces) in guts of Greylag Goose (Additional file 2: Table S1). The Aspergillus could produce ochratoxin (i.e., cancerogen; Cafsi et al 2020) and the Talaromyces induces enterobrosis (Zhao et al 2020) for human beings. Thus, the intestinal pathogens in poultry might affect the health of human beings.…”

Mycotoxins in Poultry Feed and Feed Ingredients from Sub-Saharan Africa and Their Impact on the Production of Broiler and Layer Chickens: A Review

“…In addition, the toxicity of OTA has been reported to cause impairment of the gastrointestinal tract in chickens, resulting in poor nutritional absorption and hence poor growth rate [ 68 ]. Reduced BW and BW gain were observed in broiler chickens fed OTA at levels of 20 or 50 μg/kg BW [ 82 , 101 ] or 100 to 800 μg/kg feed [ 83 , 84 ], with the difference between the FCR of the group fed control and OTA-contaminated diets increasing by about 19% after 13 days of feeding in one of the studies [ 101 ]. Feeding ZEN-contaminated diets at levels of 2000 μg/kg feed was reported to reduce BW gain and increase FCR in broiler chickens [ 65 ].…”

“…Recently, high liver and intestinal lesion scores were observed in broiler chickens fed DON (19,300 μg/kg feed) [ 80 ], and feeding FBs (50,000 or 200,000 μg/kg feed) also caused liver histological changes in broiler chickens [ 70 ]. Additionally, intestinal pathogenicity of OTA (20 or 50 μg OTA/kg body weight per day) was associated with changes in the intestinal morphology of broiler chickens characterized by lesions [ 82 , 101 ]. Furthermore, immunosuppressive effects of 2000 μg OTA/kg feed were linked to histopathological changes observed in the thymus and bursa of broiler chickens [ 67 ].…”

Tryptophan Attenuates the Effects of OTA on Intestinal Morphology and Local IgA/IgY Production in Broiler Chicks

“…The harmful effects of OTA on intestinal mucosa observed in the current study with a single dose may be due to: (a) the high dose used considering the primary local absorption (40% is passively absorbed in the upper part of the GIT), throughout the non-absorbed toxins and also by enterohepatic circulation, increasing exposure of the entire intestine [24]; (b) chick age, as newly hatched chicks do not yet have a fully developed small intestine [26]; (c) exposure route used, by gavage, which could contribute to greater OTA exposure at the GIT. According to [15,16], absorption can be decreased if it occurs together with feed consumption.…”

“…Its molecular weight is 403.82, and it is considered a weak organic acid, with a crystalline, solid, transparent, and odorless structure [1][2][3]. This mycotoxin is quickly absorbed by the small intestine in birds [15,16]. OTA affects the gastrointestinal tract (GIT) through inflammatory response/oxidative stress and by decreasing villus height [7,17].…”