Pathogenetic effects of feed intake containing of fumonisin (Fusarium verticillioides) in early broiler chicks and consequences on weight gain.

Fusarium verticillioides is often responsible for contamination of poultry feed with the mycotoxin fumonisin. The objective of the study was to determine whether fumonisin-contaminated feed in the early phase of broiler chicks causes oxidative imbalances and interferes with weight gain. One-day-old male Cobb 500 broiler chicks (n = 80) were divided into four treatments of 20 birds each, all of which were fed basal feed until the 11th day of age. From day 12, some birds were challenged with fumonisin in the feed: Control (T0) continued receiving the basal ration; treatments T1, T2, and T3 were given feed experimentally contaminated with fumonisin at concentrations of 2.5 ppm, 5 ppm and 10 ppm, respectively. After the 5th (day 17) and 10th (day 21) days, ten birds from each treatment were euthanized for blood and tissue collection to measure histopathological, biochemical and oxidative stress markers. All animals were weighed individually at the beginning of the experiment (day 12), and at 17 and 21 days of age. Birds that ingested 10 ppm of fumonisin (T3) had lower (P < 0.05) weight gain compared to those in T0. At 21 days, the body weights of the T1, T2 and T3 chicks were 1.3%, 8.97% and 18.7% lower, respectively, than those of T0. No histological lesions in the livers were observed for any treatment; however, higher levels of reactive oxygen species (ROS: day 21) and lipoperoxidation (LPO: days 17 and 21) were observed, associated with lower liver activity of the enzymes superoxide dismutase (SOD: day 21), glutathione peroxidase (GPx: day 17 and 21) and glutathione S-transferase (GST: day 21) when birds consumed 5 or 10 ppm of fumonisin. In serum, LPO levels and SOD and GPx activities were lower for groups consuming high doses of fumonisin in the diet (T2 and T3); ROS levels and GST activity were higher in these birds. Birds that consumed fumonisin-containing diets had lower levels of alanine aminotransferase, total protein and albumin (T3); as well as lower serum glucose levels (days 17 and 21), uric acid and triglycerides (day 21) in T3 than in T0. At 21 days, there were smaller crypt sizes and intestinal villi in birds that consumed high levels of fumonisin. These results suggest that fumonisin (10 ppm) in chick diet causes hepatic oxidative stress and impairs intestinal health, consequently negatively affecting weight gain.

Fumonisin-(Fusarium verticillioides)-contaminated feed causes hepatic oxidative stress and negatively affects broiler performance in the early stage: Does supplementation with açai flour residues (Euterpe oleracea) minimize these problems?

Fusarium verticillioides is often responsible for contamination of poultry feed with the mycotoxin fumonisin. The aim of this study was to determine whether oxidative stress caused by intake of fumonisin-contaminated feed affects broiler performance at an early stage of development, as well as to test whether the addition of açai residue flour to contaminated feed would minimize these negative effects of redox metabolism. Birds were divided into four groups, with four repetitions of five animals each: control (TC) - birds that received basal feed; TCA treatment - basal feed supplemented with 2% açai flour; TF treatment - feed experimentally contaminated with fumonisin (10 ppm); TFA treatment - fumonisin-contaminated feed (10 ppm) and supplemented with açai fluor (2%). The experiment lasted 20 days, that is, the first 20 days of the chicks' lives. At the end of the experiment, the birds were weighed, and blood, intestine and liver samples were collected. The TCA and TFA had greater body weights and weight gain than did TF. Further, TCA and TFA had lower feed conversion than did TF. Açai flour intake (TCA and TFA) stimulated albumin synthesis and reduced serum AST activity. Nitrate/nitrite (NOx) levels were higher in serum of fumonisin-challenged (TF) birds than in groups; NOx levels were also higher in the livers of all test groups (TF, TCA and TFA) than in TC. Serum glutathione S-transferase (GST) activity was lower in fumonisin-consuming groups (TF and TFA); this was different from what occurred in the liver, that is, higher GST activity in TF and lower activity in TFA than in TC. Catalase activity (CAT) was also higher in the fumonisin-challenged groups (TF and TFA) and the groups supplemented with açai flour (TCA) than in TC. Serum reactive species (RS) and TBARS (lipid peroxidation) levels in the liver were lower in birds supplemented with açai flour and exposed to fumonisin. These data suggest that the addition of açai flour in the feed of early chickens improves animal performance and minimizes the effects of hepatic oxidative stress in birds fed fumonisin-contaminated feed.