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PubMed1983

Evaluation of immunity of young broiler chickens during simultaneous aflatoxicosis and ochratoxicosis.

A 2 X 2 factorial experimental design consisting of the treatments 0 and 2.5 micrograms/g aflatoxin and 0 and 2.0 micrograms/g ochratoxin A with 12 replicates of 10 birds per treatment level was used to evaluate the effects of these mycotoxins on various aspects of immunity. Male chicks (Hubbard X Hubbard) were maintained on these treatments from one day of age to 3 weeks of age at which time six replicate pens per treatment were sacrificed and various parameters measured. The additional six replicate pens per treatment were maintained on toxin feed beyond 3 weeks of age, and at 4 weeks of age, three replicate pens were immunized with sheep red blood cells (SRBC) and Brucella abortus. Antibody titers were measured up to 10 days postimmunization. Aflatoxin and ochratoxin A, individually, significantly (P less than .05) decreased body weight, and a synergistic toxicity was evident by a significant (P less than .05) decrease in body weight. Antibody titers and phagocytic activity of heterophils were not significantly (P less than .05) altered by any treatments. The relative weight of the bursa of Fabricius and the number of follicles for a given area of the folds of the bursa of Fabricius were significantly (P less than .05) decreased only by the interaction treatment. Complement activity was significantly (P less than .05) decreased by aflatoxin and the combination of aflatoxin and ochratoxin A and depressed, although not significantly (P less than .05), by ochratoxin A.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1983

Histochemical analysis of liver cells from short term, aflatoxin-dosed and nondosed Coturnix coturnix japonica. 1. Aflatoxin-sensitive quail.

Although aflatoxicosis in Coturnix coturnix japonica has been described, the histochemical localization of liver chemicals and the occurrence of ingested aflatoxins within blood, feces, and liver have not been described. Six to 8-week-old quail, which were intubated with a carrier with or without .3 mg mixed aflatoxins (AFB1, AFB2, AFG1, AFG2)/kg body weight were sacrificed within .25 to 5 days of intubation. Deparaffinized sections of livers were stained for lipids, nucleic acids, polysaccharides, and proteins. Other livers and excrement were homogenized and filtered homogenates as well as blood partitioned against chloroform. The aqueous phase was treated with pepsin and then partitioned, but the organic phase was analyzed directly. Organic phases of .25 to 5 day blood, feces, and liver lacked aflatoxins. Pepsin digesta of blood from males and females dosed 6 hr appeared to contain aflatoxicol (disappeared by 24 hr) and an unknown fluorescent compound, respectively. Whereas an unidentified fluorescent compound was observed within excrement of males dosed 6 hr, female excrement contained a fluorescent compound with an AFB1 Rf (disappeared by 24 hr). Although the liver of males dosed 6 hr had three fluorescent compounds (Rfs for AFB1 and AFB2a), only one was seen within dosed females. Ultra violet absorption spectra of presumed AFB2a and aflatoxicol failed to yield their reported absorption maxima. Livers from dosed quail exhibited bile duct proliferation, cellular necrosis, vacuolization, congestion, fatty changes and mild hepatitis. Sinusoidal membranes were thickened and contained abundant periodic acid-Schiff's (PAS)-positive substances. Although livers of nondosed quail abounded with regularly shaped and uniformly distributed, Sudan IV-positive droplets, livers of dosed quail accommodated few, irregularly-shaped and positioned droplets. Hepatocyte nuclei and nucleoli of dosed quail displayed marked affinities for the Feulgen reagent and toluidine blue O, respectively. Lobules of dosed quail possessed concentrations of cells in which their entire cytoplasm was PAS positive. Treatment of sections with alpha-amylase reduced staining suggesting the presence of glycogen. Ninhydrin-positive substances were distributed throughout the liver in both DQ and non DQ with no apparent difference in intensities between the two livers. Generally the DQ showed mild hepatitis due to aflatoxicosis and the toxin altered liver histochemistry for the major classes of cellular chemicals.

Aflatoxins↗

PubMed1984

Experimental induction of chronic aflatoxicosis in chickens by purified aflatoxin B1 and its reversal by activated charcoal, phenobarbital, and reduced glutathione.

Aflatoxin B1 (AFB1) caused dose-dependent reductions in weight gain and feed consumption when day-old Hubbard X Hubbard broiler type chicks were maintained on a diet contaminated with either 0, 2.5, 5, or 10 ppm purified AFB1 for 8 weeks. Although changes in these parameters were detected at the 2.5 and 5 ppm, the most profound changes were evident at 10 ppm contamination. The concentration of cytochrome P-450 in hepatic microsomes, measured at the end of 8 weeks, also showed dose-dependent decreases. Cytochrome P-450 content in chickens receiving 2.5, 5, and 10 ppm AFB1 was 16, 28, and 65%, respectively, less than the control. Microsomal benzphetamine N-demethylase activity was not inhibited by 2.5 or 5 ppm, but ingestion of 10 ppm AFB1 reduced its activity by more than 40%. Serum glutamic oxalacetic transaminase (SGOT) levels of chickens receiving 10 ppm AFB1 increased by more than 100%, indicating substantial liver damage. However, birds simultaneously receiving 10 ppm AFB1 and activated charcoal (.1% in the feed) or either reduced glutathione (.05%) or phenobarbital (.05%, given intermittently) in their drinking water showed a trend of improvement in feed consumption (less than 10% reversal) and weight gain (less than 28% reversal) over the birds receiving 10 ppm AFB1 alone. The results also indicate that the simultaneous presence of these agents with AFB1 considerably prevented the inhibitory effect of AFB1 on the microsomal cytochrome P-450 and benzphetamine N-demethylase activity. Furthermore, these agents were able to provide moderate protection against AFB1-induced liver injury manifested by elevation of SGOT activity.

Aflatoxin B1↗

PubMed1986

Relative importance of dietary aflatoxin and feed restriction on reproductive changes associated with aflatoxicosis in the maturing White Leghorn male.

A study was conducted to investigate the relative contribution of dietary aflatoxin and feed restriction on reproductive and endocrine changes associated with aflatoxicosis. Pair-feeding was used to factor out nutritional and toxicological effects of aflatoxin on reproduction in the maturing White Leghorn male. Birds were randomly assigned to treatment groups at 9 weeks and fed experimental diets for 3 weeks. Experiment 1 involved the partitioning of toxicological and nutritional effects of aflatoxin on both physiological and reproductive parameters. Aflatoxin-fed males had significantly greater relative liver weights and liver lipid content than control or pair-fed males; no differences in testicular weights were found among treatments. Plasma testosterone levels in controls were significantly higher than in pair-fed birds; aflatoxin-treated males exhibited the lowest concentrations. Pituitary and testicular responsiveness to synthetic luteinizing hormone-releasing hormone (LHRH) were monitored in Experiment 2. Plasma luteinizing hormone (LH) levels in aflatoxin-fed males were significantly higher than in control or pair-fed males prior to LHRH administration. Additionally, the LH response of pair-fed birds to exogenous LHRH was qualitatively different from that observed in the other two treatments; this indicates that hormonal changes observed during aflatoxicosis and feed restriction are a result of different physiological mechanisms. Plasma testosterone also increased after LHRH injection. This response was significantly greater in controls than in pair-fed males, and nonexistent in aflatoxin-treated birds.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Enhanced production of pancreatic digestive enzymes during aflatoxicosis in egg-type chickens.

As aflatoxin causes malabsorption and its toxicity is enhanced by a low protein diet, digestive enzymes formed in the pancreas apparently are influenced by aflatoxin. This hypothesis was investigated in a 2 X 2 factorial experiment. Six groups of 10 egg-type chickens per treatment were analyzed for the absence and presence of aflatoxin (0 and 4 micrograms/g diet) and for normal (12.75%) and low (10.00%) protein in soy-dextrose diets. The specific activities of pancreatic chymotrypsin, amylase, and lipase, but not trypsin, were increased significantly (P less than .01) by aflatoxin. Lowering dietary protein had no effect by itself except to increase amylase activity. Low protein and aflatoxin interacted to lessen but not prevent the effect of aflatoxin on chymotrypsin and amylase. Calculation of total pancreatic activities revealed that aflatoxin increased trypsin, chymotrypsin, amylase, and lipase to 107, 169, 113, and 119%, respectively, of control values on the low protein diet, whereas values were 99, 175, 115, and 115%, respectively, on the normal protein diet. Neither aflatoxin nor low protein altered significantly (P less than .05) the lipid content of fecal material. Thus, aflatoxicosis in egg-type chickens is characterized by a surplus of some digestive enzymes and by normal fecal lipids in contrast to the specific deficiency of amylase and lipase and steatorrhea reported earlier in meat-type chickens. Whereas malabsorption caused by aflatoxin in broilers can be accounted for in part by impaired digestion, this mechanism apparently does not occur in egg-type chickens.

Animals↗

PubMed1987

Interaction of dietary protein level on dose response relationships during aflatoxicosis in young chickens.

It is well known that the effect of aflatoxin is enhanced by a low protein diet, but whether this is associated with a lower apparent minimum effective dose, increased slope of response curves, or both has not been investigated previously. Aflatoxin at 12 dosages ranging from 0 to 2.34 micrograms/g of feed was fed to eight groups of 10 young chickens per treatment consuming a 10.00 or 12.75% protein diet for 3 weeks. The body weights, liver weights relative to body weights, and total lipid content of the livers were determined. Mathematical models were fitted to the data and from the appropriate equations the dose-response curves were predicted as continuous functions of aflatoxin concentration. A quadratic polynomial fit body weight data on the 12.75% protein diet whereas a plateau-linear model fit body weight data on the 10.00% protein diet. This implies that in a low protein diet aflatoxin affects only one of the factors controlling growth. Plateau-linear models fit liver relative weight and liver lipid content data on both 10.00 and 12.75% diets. For both variables the lower protein diet decreased the apparent minimum effective dose and increased the positive slope of the linear response. The apparent minimum effective doses (micrograms of aflatoxin per gram of feed) in this experimental system were calculated from the modeling approach to be 1.21 and 2.00 for body weight, 1.08 and 1.65 for liver lipids, and 1.45 and 2.34 for liver relative weight in 10.00 and 12.75% protein diets, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxins↗

PubMed1987

Altered metabolism of carotenoids during aflatoxicosis in young chickens.

Young chickens were fed from hatching until 3 weeks of age with a white corn-soy diet (containing 1.36 micrograms total carotenoids per gram of diet) amended with a commercial preparation of lutein, a dihydroxycarotenoid, to supply 25 micrograms free lutein per gram diet. The diet which also contained 0, 1, 2, 4, or 8 micrograms aflatoxin per gram of diet was fed to four groups of ten chickens per aflatoxin treatment until they were 3 weeks old. Aflatoxin had no effect on the partial acylation of free lutein to lutein monoester that occurs in the jejunal contents of normal birds but it decreased significantly (P less than .05) the conversion of free lutein to lutein diester. Aflatoxin reduced up to 35% the lutein (94% free alcohol) content of the jejunal mucosa and the serum lutein (99% free alcohol) was reduced by up to 70%. Aflatoxin caused a slight (25%) decrease in the free lutein content of liver while increasing the monoester content 3.5-fold and the diester content 10-fold. This sequestering of lutein in the liver in esterified forms poorly transported to the integument presumably contributes to the poor pigmentation during aflatoxicosis. The forms of lutein in the toe web were diester (66%0, free alcohol (26%), and monoester (8%) and their sensitivity to aflatoxin followed the same order. These data offer clear, unequivocal proof that aflatoxin can cause poor pigmentation in birds, presumably by interfering with the absorption, transport, and deposition of carotenoids.

Aflatoxins↗

PubMed1987

Influence of avian aflatoxicosis on the synthesis of polyamines.

Effects were examined of inanition, dietary aflatoxin (2.5 mg/kg), and dietary supplements of threonine, lysine, and arginine on the activities of renal arginase and hepatic ornithine decarboxylase and on the accumulation of polyamines in liver and brain of 24 or 26-day-old broiler cockerels. Aflatoxicosis and inanition lowered the activity of renal arginase by 58 and 37%, respectively. Supplemental dietary threonine (.4%) did not suppress the activity of renal arginase, while fortification of diets of controls with lysine (.53%), but not diets containing aflatoxin, elevated the activity of renal arginase. Supplements of dietary lysine and/or arginine did not influence the hepatic content of putrescine but lowered the concentrations of spermidine and spermine. Aflatoxicosis, but not inanition, increased the activity of hepatic ornithine decarboxylase (ODC; 22-fold), increased hepatic concentrations of putrescine and spermidine, but decreased spermine concentrations. The elevation of hepatic ODC, putrescine, and the ratio of spermidine to spermine parallels the enlargement of the liver caused by aflatoxicosis. Cadaverine and putrescine were not detected in avian brain, while cerebral concentrations of spermidine and spermine were not altered by aflatoxin, inanition, or by supplements of dietary lysine, arginine, or both lysine and arginine.

Animals↗

PubMed1987

Effect of dietary fat level on dose response relationships during aflatoxicosis in young chickens.

The effect of aflatoxin in poultry is greater on birds fed a low fat diet, but it is not known whether this effect is associated with a lower apparent minimum effective dose (MED), altered slope of the response curve, or both. Aflatoxin at 16 dosages ranging from 0 to 3.797 micrograms/g of feed was fed to six groups of 15 young chickens per treatment ingesting a 2 or 4% fat diet for 3 wk. The weights of the body, liver, bursa of Fabricius, and spleen and the total lipid content of the liver were measured. Mathematical models were fitted to the data and dose-response curves were predicted as continuous functions of aflatoxin concentration. Quadratic polynomials fit body weight and spleen weight whereas plateau-linear models fit liver weight and liver lipid content in both 2 and 4% fat diets. The weight of the bursa of Fabricius was fit equally well by quadratic and linear plateau models. Dietary fat had negligible effects on the apparent MED (micrograms of aflatoxin per gram of feed) for body, liver and spleen weights, which were calculated from the modeling approach to be 1.37 and 1.41, 1.68 and 1.69, and 1.49 and 1.46 on 2 and 4% fat diets, respectively. The apparent MED for liver lipid content was appreciably lower for birds fed the 2% fat diet than those fed the 4% fat diet (.88 and 1.62, respectively). Similarly, the apparent MED for the bursa was 1.48 and 1.74 for birds fed the 2 and 4% fat diets, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxins↗

PubMed1987

Selection for resistance to aflatoxin in chickens.

Two populations of broiler chickens [Athens-Canadian (AC) and a commercial stock] were selected for resistance to aflatoxicosis by dosing chickens in each population with a single oral dose of aflatoxin, which resulted in 40 to 70% mortality. Chickens that did not receive aflatoxin served as the nonselected control groups. Birds surviving the aflatoxin challenge were used as breeders for subsequent generations. Rapid progress was made in the AC population for resistance to aflatoxin, but only moderate progress for this trait was attained in the commercial broiler stock. After five generations of selection in the AC population, LD50 values of 9.42 and 17.05 milligrams aflatoxin per kilogram body weight (BW) were determined for the nonselected and selected lines, respectively. After four generations of selection in the commercial broiler population, LD50 values of 6.05 and 8.02 mg aflatoxin/kg BW were determined for the nonselected and selected lines, respectively. These data demonstrate that genetic progress can be made in chickens, but the amount of progress for resistance to aflatoxin may be influenced by the population.

Animals↗

PubMed1987

Increased sensitivity to staphylococcal beta hemolysins of erythrocytes from chickens during aflatoxicosis.

The size of the zones of beta-hemolysis surrounding staphylococcal colonies on blood agar was found to be related to the level of dietary aflatoxin consumed by the chickens donating the blood. Zone sizes on blood from chickens fed the highest level of aflatoxin (10 micrograms/g of diet) were about six-fold larger than those on blood from control birds. The percentage of staphylococcal isolates displaying beta-hemolysis was increased from about 15% in normal blood to about 90% in blood from chickens fed aflatoxin (10 micrograms/g) whereas the time required for detection of beta-hemolysis was decreased by about one-half. The hemolytic activity of purified staphylococcal beta-hemolysin against suspensions of washed erythrocytes increased as the level of aflatoxin consumed by the donor chickens increased. These data imply a new mechanism for enhanced susceptibility of animals to infectious agents during mycotoxicoses whereby the animal is made more sensitive to the virulence factors of pathogens.

Animals↗

PubMed1987

Metabolism of lutein diester during aflatoxicosis in young chickens.

Young chickens were fed from hatching until 3 wk of age with a white corn-soy diet amended with lutein diester to supply 25 micrograms lutein/g diet and with varying amounts of aflatoxin (0, 1, 2, 4, and 8 micrograms/g diet). The lutein diester was added as a stabilized, microencapsulated extract of marigold (Tagetes erecta) petals. Aflatoxin had no significant effect on the partial conversion of lutein diester to lutein monoester and lutein that occurs in the jejunum of normal chickens. The concentration of lutein in the jejunal mucosa was increased slightly by intermediate levels of aflatoxin and depressed by higher levels. Aflatoxin depressed lutein (the dominant form) in serum by up to 40%. Aflatoxin enhanced the lutein accumulation in the liver as the monoester (four-fold) and diester (12-fold). Only minor effects of aflatoxin on the carotenoid content of the toe webs were noted in birds fed lutein diester. These results imply that the main effects of aflatoxin on the utilization of lutein diester are to impair the absorption of lutein, which is an intestinal product of dietary lutein diester, and to sequester lutein as lutein monoester and lutein diester in the liver.

Animals↗

PubMed1988

Hydrated sodium calcium aluminosilicate: a high affinity sorbent for aflatoxin.

Aluminas, silicas and aluminosilicates were evaluated for their ability to sorb radiolabeled aflatoxin B1 (AFB1) from aqueous solution (in vitro). Hydrated sodium calcium aluminosilicate (HSCAS) was selected for testing in vivo due to its high affinity for AFB1, because of its stable association with AFB1, and its GRAS (generally recognized as safe) status as an anticaking agent. The HSCAS, when added to the diet of Leghorn and broiler chicks at a level of .5%, significantly diminished the adverse effects of feeding 7.5 mg AFB1/kg of feed. Thus, this agent (and other aluminosilicate congeners) may prove effective in the preventive management of aflatoxicosis.

Absorption↗

PubMed1990

Effect of dietary lipid on lutein metabolism during aflatoxicosis in young broiler chickens.

The effect of concentration of dietary fat on pigmentation of broiler chickens was investigated in diets containing: 1) 0 or 1.4 micrograms of aflatoxin and 35 micrograms of lutein/kcal of diet; and 2) different levels of dietary fat (0, 2, 4, 6, 8, or 10% cottonseed oil). Serum lutein and its metabolite, 3'-oxolutein, increased with increasing dietary fat until it reached a plateau at 6% fat. Aflatoxin significantly (P less than .05) lowered serum lutein and 3'-oxolutein at all levels of fat. Dietary fat and aflatoxin interacted significantly (P less than .05), with the effect of aflatoxin being greater at the low levels of fat than at the high fat levels. In the toe webs of the birds, the concentrations of lutein and its metabolites, lutein monoester, lutein diester, and 3'-oxolutein responded similarly to aflatoxin and to dietary fat, except that increasing the amount of dietary fat did not spare the effect of aflatoxin on 3'-oxolutein. The effect of chain length and the saturation of fatty acids on the absorption of lutein during aflatoxicosis was investigated in a factorial design for aflatoxin (0 and 4 micrograms/g of diet) and seven fatty acids at 5% of the diet. In control birds, lutein absorption was promoted by lauric = oleic greater than capric = linoleic greater than myristic greater than palmitic = stearic acids. Aflatoxin significantly (P less than .05) depressed the absorption of lutein regardless of the fatty acid present.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗

PubMed1990

Effect of cold acclimation on the broiler chicks' resistance to acute aflatoxicosis.

The effect of acclimation to environmental temperatures of 10 to 12, 14 to 16, or 28 to 30 C on the resistance of broiler chicks to acute aflatoxicosis was studied in a series of four experiments. Chicks acclimated to 10 to 12 C were more resistant to a single oral dose of aflatoxin (8 mg per kg of BW) after 10 and 20 days than chicks acclimated to 28 to 30 C. However, chicks acclimated to 14 to 16 C required 20 days of acclimation before an increase in resistance was observed. Acclimation to 10 to 12 C for 14 days followed by acclimation to 28 to 30 C for 7 days resulted in no increase in the resistance of the chicks to an aflatoxin dose (8 mg per kg of BW) at 21 days, indicating that the resistance conveyed by cold acclimation was temporary. Sodium-pentobarbital sleeping time was significantly decreased and the cytochrome P-450 content was significantly increased after acclimating broiler chicks to 10 to 12 C. These observations suggest that stimulation of the microsomal mono-oxygenase system after cold acclimation may be responsible for the increased resistance of the broiler chick to acute aflatoxicosis.

Acclimatization↗

PubMed1990

Diminution of aflatoxicosis in growing chickens by the dietary addition of a hydrated, sodium calcium aluminosilicate.

The amelioration of aflatoxicosis in broiler and Leghorn chickens was examined by feeding a hydrated, sodium calcium aluminosilicate (HSCAS) or activated charcoal. In three experiments, HSCAS or activated charcoal at a concentration of .5% of the total diet were incorporated into diets for broiler and Leghorn chicks containing either no added, purified aflatoxin B1 (AFB1), 7.5 mg of AFB1 per kg, or 5 mg of aflatoxin (AF) per kg (produced by Aspergillus parasiticus on rice). Compared to the controls, the AFB1 reduced BW gains at 0 to 3 wk by 21 to 38% in broilers; and the AF reduced BW gains at 0 to 4 wk in Leghorns by 20 percent. The HSCAS significantly diminished the growth-inhibitory effects of AFB1 or of AF on growing chicks by 50 to 67 percent. Feeding 5 mg of AF per kg of diet with or without charcoal to Leghorn chicks caused a significant increase in the relative weights of the liver, kidney, proventriculus, and gizzard as well as significant increases in activity of serum gamma glutamyltransferase; also, significant decreases in the relative bursa weights as well as the concentrations of serum total protein and albumin. With the exception of the relative bursa weights, the toxic effects caused by aflatoxin were prevented or were reduced by adding hydrated, sodium calcium aluminosilicate. These data suggest that HSCAS can modulate the toxicity of AFB1 and AF in the chicken; however, adding activated charcoal to the diet did not appear to have protective properties against the effects of aflatoxin B1 or of aflatoxin.

Aflatoxin B1↗

PubMed1990

Effect of cold acclimation on the broiler chicks' resistance to dietary aflatoxin.

The effect of acclimation to environmental temperatures of 10 to 12 or 28 to 30 C on the resistance of broiler chicks to dietary aflatoxin was examined. Broiler chicks were acclimated from day-of-age for 2 wk to environmental temperatures of 10 to 12 or 28 to 30 C. On Day 14, a single oral dose of aflatoxin (8 mg per kg of body weight) was administered to 50 chicks in each environment. An increase in aflatoxin resistance, as assessed by survival rate, was conveyed by acclimation to cold temperatures. In each environmental chamber, a separate group of chicks was maintained for 2 additional wk, but those groups received 5 mg of aflatoxin per kg feed. By the end of the study, aflatoxicosis was characterized by: 1) a significant (P less than or equal to .05) decrease in body weight; 2) increases in spleen weight, liver weight, liver lipid, and liver dry-matter content; 3) changes in the serum levels of total protein, albumin, glucose, cholesterol, uric acid, potassium, phosphorus, iron and calcium; and 4) increased hepatic hyperplasia. Acclimation to 10 to 12 C was characterized by: 1) an increase in body weight, liver weight, spleen weight and bursa weight; 2) changes in the serum glucose and potassium levels; and 3) a decrease in glutamic-oxaloacetic transaminase activity. Significant aflatoxin by temperature interactions were evident only in serum levels of glucose and phosphorus, and in the serum activity of glutamic-oxaloacetic transaminase. These data suggest that acclimation to cool temperatures does not play a significant role in the resistance by broiler chickens to chronic aflatoxin exposure.

Adaptation, Physiological↗

PubMed1990

Altered renal function in broilers during aflatoxicosis.

Experiments were conducted to determine the effects of aflatoxicosis on acid-base balance, urine flow rate (V), glomerular filtration rate (GFR), clearance of para-aminohippuric acid (CPAH), plasma osmolality, and the renal handling of Na, K, Ca, and P. Three-week-old broilers were gavaged with aflatoxin at a dose of 2 mg/kg of BW per day for 10 consecutive days. Control birds received an equal volume of corn oil, the aflatoxin carrier vehicle. On the eleventh day, the birds were anesthetized and prepared for renal function analysis. A solution containing inulin, para-aminohippuric acid, and mannitol was infused at a low infusion rate (.1 mL/kg of BW per min) and a high infusion rate (.4 mL/kg of BW per min) to determine if aflatoxin affects the renal response to an acute volume load. Aflatoxicosis decreased the fractional excretion of phosphorous (FEP) and plasma Ca concentration but did not significantly alter any other renal function or acid-base variables. The decrease in FEP and plasma Ca may be a direct result of renal tubular damage, decreased Ca absorption from the gut, or a result of altered circulating levels of parathyroid hormone (PTH), and possibly decreased renal sensitivity to PTH.

Animals↗