Biomedical subjects

W M Hagler

Publications and source records attributed to W M Hagler.

At least 19 recordsLinked to original sources

PubMed1999

Cytosol is required for the modulation by dietary casein of the hepatic microsomal activation of aflatoxin B1 to mutagenic metabolites detectable in Salmonella.

We have shown previously that dietary protein (casein) levels can affect the ability of rat liver S9 to metabolize aflatoxin B1 (AFB) as well as other promutagens detectable in Salmonella strain TA98 [Mutat. Res. (1997), 360, 115-126 and 127-143]. The mutagenic potency of AFB was greatest when metabolized by the Aroclor 1254-induced hepatic S9 prepared from F344 male rats that consumed an isocaloric, semisynthetic diet for 6 weeks that contained an adequate (12%) level of methionine-supplemented casein as the sole protein source, compared with S9s from rats fed diets that contained nominally deficient (8%) or high (22%) levels of casein. Here we have extended this observation by performing (i) mutagenicity studies with microsomes, cytosols and reconstituted S9s (recombinations of microsomes and cytosols across dietary groups), and (ii) in vitro incubations followed by analysis of metabolites by fluorescence high-pressure liquid chromatography. Microsomes, but not cytosols, activated AFB; however, activation to the level observed with S9 occurred only when microsomes from the rats fed 12% casein were combined with cytosols from any dietary group. Consistent with the mutagenicity results, the greatest metabolism of the AFB parent compound and the highest level of the glutathione conjugate of the presumptively identified AFB-exo-8,9-epoxide (the ultimate mutagenic form of AFB) were produced by S9s from the rats fed the 12% casein diet. The levels of these metabolites and the mutagenicity of AFB changed in parallel with changes in dietary casein levels. In summary, cytosolic elements, which are not affected by dietary casein levels, interact with microsomal enzymes, which are modulated by dietary casein levels, to influence the ability of hepatic S9 to activate AFB to a mutagen.

Aflatoxin B1↗

PubMed1998

Dietary exposure of broiler breeders to aflatoxin results in immune dysfunction in progeny chicks.

Broiler breeder hens were fed diets amended with 0 and 10 mg/kg (Trial 1) or 0, 0.2, 1, or 5 mg/kg (Trial 2) of aflatoxin (AF). Fertile eggs collected during 14 d of AF feeding were examined for AF residues. Various immunological endpoints were examined in chicks hatched from these eggs. Eggs collected at 7 d of AF feeding (Trial 1) had 0.15 to 0.48 ng/g of AFB1 and 0.22 to 0.51 ng/g of aflatoxicol, whereas eggs collected at 14 d of AF feeding had 0.05 to 0.60 ng of AFB1/g and 0.19 to 1.20 ng of aflatoxicol/g. In both trials, AF dietary exposure resulted in embryonic mortality and reduction in hatchability compared to controls. The AF progeny chicks in Trial 2 had total anti-SRBC antibodies similar to the controls during the primary antibody response. However, at 5 and 7 d after secondary SRBC injection, the antibody levels in the 1 and 5 mg/kg AF groups were lower than those of controls. Depression in anti-Brucella abortus antibodies occurred only in chicks from the 5 mg/kg AF group. Furthermore, phagocytosis of SRBC and reactive oxygen intermediate production by macrophages from AF progeny chicks were reduced as compared with the control chicks. The findings of this study imply that the progeny chicks from hens consuming a AF-amended diet may be increasingly susceptible to disease owing to suppression of humoral and cellular immunity.

Aflatoxin B1↗

PubMed1997

T-2 tetraol is cytotoxic to a chicken macrophage cell line.

Cytotoxic effects of T-2 tetraol, a T-2 toxin derivative, on the MQ-NCSU chicken macrophage cell line were quantified by direct in vitro exposure. Macrophage cultures were exposed to 1, 10, 20, 40, 80, 160, and 320 micrograms/mL of T-2 tetraol for 1 h. Macrophage viability after exposure to T-2 tetraol. Macrophage viability was reduced by increasing concentrations of T-2 tetraol (linear effect, P < or = 0.001; quadratic effect, P < or = 0.025). The ability of macrophages to adhere to glass surfaces was impaired by increasing concentrations of T-2 tetraol (linear effect, P < or = 0.003). This experiment demonstrates that T-2 tetraol is cytotoxic to chicken macrophages in vitro.

Animals↗

PubMed1996

Degradation of aflatoxin by poultry litter.

Two trials were conducted to determine whether deep stacking of contaminated corn with poultry litter destroys aflatoxin. Contaminated corn was ground and mixed with litter to carbon:nitrogen ratios of 30:1. Moistures were adjusted by adding tap water just prior to incubation or stacking. The initial laboratory trial included only broiler litter at 40% moisture, whereas the subsequent field trial involved a 2 x 2 factorial design with litter type (turkey or broiler) and moisture (20 or 40%) as main effects. Aflatoxin assays were reduced in the laboratory trial from 433 and 402 to 54 and 8 ppb in Containers 1 and 2, respectively, after 35 d of incubation at 28 C. In the field trial, aflatoxin disappeared from broiler and turkey litter mixtures with projected moistures of 20% after 10 and 6 wk of storage, respectively, whereas disappearance in mixtures containing projected moistures of 40% required 5 and 3 wk, respectively. Differences in moisture appear to account for differences in the ability of turkey and broiler litter to detoxify aflatoxin. Hence, turkey and broiler litter would appear equal with respect to the ability to detoxify aflatoxin-contaminated corn. Disappearance of aflatoxin during storage with litter could have occurred as a result of ammonia release during storage or microbial detoxification mechanisms. However, nitrogen values suggest that microbial action was responsible for much of the detoxification, as aflatoxin disappeared from mixtures with little apparent ammonia release.

Aflatoxins↗

PubMed1995

Fusaric acid in Fusarium moniliforme cultures, corn, and feeds toxic to livestock and the neurochemical effects in the brain and pineal gland of rats.

Fusaric acid is produced by several species of Fusarium, which commonly infect corn and other agricultural commodities. Since this mycotoxin may augment the effects of other Fusarium toxins, a gas chromatography/mass spectrometry method of analysis in feeds was developed. Fusaric acid was analyzed as the trimethylsilyl-ester from F. moniliforme-cultures, -contaminated corn screenings, and feeds toxic to livestock. The mycotoxin was found in all samples and ranged from 0.43 to 12.39 micrograms/g sample. Also, fusaric acid was tested for its neurochemical effects in the brain and pineal gland of rats. Animals were dosed intraperitoneally (100 mg/kg body weight) 30 min prior to the onset of the dark phase (lights out) and the effects were studied at 1.5, 3.5, and 5.5 h after treatment. Brain serotonin (5HT), 5-hydroxyindoleacetic acid (5HIAA), tyrosine (TYRO), and dopamine (DA) were increased (P < 0.05) by fusaric acid, and norepinephrine (NEpi) was decreased (P < 0.05). Analogously, DA in the pineal gland increased and NEpi decreased (P < 0.05). Pineal N-acetylserotonin (NAc5HT) was increased (P < 0.05), whereas pineal 5HT and its two major metabolites 5HIAA and 5-hydroxytryptophol (5HTOL) decreased (P < 0.05). Elevated brain TYRO and brain and pineal DA, with decreased NEpi, may be consistent with fusaric acid's partial inhibitory effect on tyrosine-hydroxylase and its inhibitory effect on dopamine-beta-hydroxylase, respectively. Elevated pineal Nac5HT is consistent with decreased pineal 5HT and the increased pineal DA, and support the dopaminergic stimulatory activity of the enzyme responsible for the conversion of 5HT to NAc5HT. This is the first report of fusaric acid's in vivo effect on pineal DA, NEpi, 5HT, and NAc5HT in rats, and a relation for the effects on TYRO, 5HT, and 5HIAA in brain tissue. The results indicate fusaric acid alters brain and pineal neurotransmitters and may contribute to the toxic effects of Fusarium-contaminated feeds.

Animal Feed↗

PubMed1995

Influence of duodenal slaframine infusion on site of nutrient disappearance from the digestive tract of steers fed a high-concentrate diet.

The effect of duodenal slaframine (SF) infusion on site and extent of digestion was determined using four steers equipped with ruminal, duodenal, and ileal cannulas in a 4 x 4 Latin square. A 77% dry-rolled corn diet was provided in 12 equal portions daily at a DMI of 2.26% BW. Slaframine in a .9% saline excipient was infused into the duodenum every 12 h with total daily dose of 0, 30, 60, or 90 micrograms /kg of BW. Slaframine infusion had no effect on ruminal pH, ruminal NH3 N, or solids and liquids passage rate. Slaframine increased (linear, P < .10) total tract OM and starch disappearance and digestibility and tended to increase (linear, P = .14) total tract N digestibility. Ruminal starch disappearance tended to be decreased (quadratic, P = .16) by SF. Small intestinal OM digestibility was increased (linear, P < .10) but starch digestibility in the small intestine was not affected by SF. Increased total tract starch digestibility was caused by increased (quadratic, P < .10) starch fermentation in the large intestine. Ruminal feed N digestibility decreased at the intermediate doses of SF (quadratic, P < .10). Total N digestibility in the small intestine tended to be increased (cubic, P = .13) with 30 and 90 micrograms of SF/kg of BW. Decreased ruminal feed N digestion was compensated for by increased (quadratic, P < .10) small intestinal feed N disappearance for steers treated with intermediate doses of SF. The potential of SF to increase starch digestion in the rumen and small intestine seems to be limited.

Alkaloids↗

PubMed1995

Endocrine and metabolic response to muscarinic stimulation and inhibition in the ruminant: effects of slaframine.

The influence of slaframine (SF), a parasympathomimetic compound isolated from the fungus Rizoctonia leguminicola, on circulating metabolic hormone concentrations was investigated in goats. In Exp. 1, SF was administered i.v. at 0 (CONT), 50 (LSF), 100 (MSF), or 150 (HSF) microgram/kg.75 BW in four mature Spanish-cross does (average BW 36 +/- 7 kg) fitted with indwelling jugular vein catheters in a 4 x 4 Latin square design. Plasma glucose peaked (P < .06) at 120 min with LSF and at 180 min with HSF and was higher (P <.06) than the CONT at these times. Glucose exhibited a quadratic response (P < .03) to SF. Area under the response curve for glucose differed (P < .02) in HSF from CONT and MSF. Insulin peaked (P < .01) at 240 min with MSF and at 180 min with HSF. Plasma triiodothyronine was maintained at a higher level (P < .03) with HSF. Thyroxine peaked (P < .06) at 120 min with MSF and 300 min with HSF. Plasma NEFA and somatotropin concentrations were not affected (P > .10) by SF. In Exp. 2, four mature Spanish-cross wethers (average BW 27 +/- 2 kg) fitted with jugular vein catheters were administered SF (0 and 114 micrograms/kg.75 BW) and 4-diphenylacetoxy-N-methylpiperidine methiodide (4DAMP; 0 and 258 micrograms/kg.75 BW), a M3-muscarinic receptor antagonist, i.v. in a 4 x 4 Latin square design with a 2 x 2 factorial arrangement of treatments. With SF, glucose peaked (P < .06) at 60 min and insulin peaked (P < .05) at 180 min. Plasma triiodothyronine levels were maintained (P < .05) with SF but declined with other treatments. Plasma NEFA and thyroxine concentrations remained unchanged regardless of treatment. Slaframine administration induced hyperglycemia and hyperinsulinemia in goats; however, these changes were blocked by preadministration of isomolar quantities of the M3-muscarinic receptor antagonist, 4DAMP.

Alkaloids↗

PubMed1995

The effect of slaframine on salivary output and subacute and acute acidosis in growing beef steers.

Experiments were conducted to determine 1) the effect of injecting slaframine (SF) on salivary output in growing beef steers and 2) whether increased salivary output after SF injection would inhibit the decrease in ruminal pH that occurs after experimentally induced subacute and acute ruminal acidosis. In Exp. 1 and 2, we measured ruminal pH and salivary output in ruminally and esophageally cannulated beef steers fed an 88% concentrate diet. Injections of 66 or 100 micrograms of SF/kg BW increased salivary flow approximately 50% compared with controls. Those doses were tested in subacute and acute acidosis models using ruminally cannulated beef steers in Exp. 3 and 4, respectively. In these experiments, salivation was assessed indirectly using a visual scoring system. In the subacute acidosis model, SF reduced (P < .10) the decrease in ruminal pH (1.1, .7, and .6 pH units for control, 66, and 100 micrograms of SF/kg BW doses, respectively), and excessive salivation was observed in all SF-injected steers. In the acute acidosis model, there were no differences (P > .10) in ruminal pH at 12 h after injection between control and SF-treated steers. Mean ruminal lactate concentrations for all treatment groups were between 87 and 112 mM. Although treatment with 66 micrograms of SF/kg BW reduced (P < .10) ruminal lactate concentrations, all ruminal lactate concentrations were indicative of acute acidosis. These results indicate that SF will reduce the decrease in ruminal pH associated with subacute acidosis in growing beef steers, but SF does not attenuate acute ruminal acidosis.

Acidosis↗

PubMed1995

The involvement of slaframine and swainsonine in slobbers syndrome: a review.

The history of "slobbers syndrome," a mycotoxicosis associated with Rhizoctonia leguminicola infestation of pastures and stored forages, is discussed. The chemistry and physiological effects of the two known biologically active alkaloids of R. leguminicola, slaframine and swainsonine, are described. Slaframine administration is generally associated with increased exocrine function, especially salivation. Ingestion of swainsonine may be linked to serious and potentially lethal central nervous system defects similar to that described for locoism. However, the singular effects of these alkaloids do not completely account for the total clinical picture noted in the field during the occurrence of slobbers syndrome. It is possible that this phenomenon is the result of an interaction between both known and unidentified biologically active metabolites of R. leguminicola.

Alkaloids↗

PubMed1995

Trichothecene mycotoxins depress the mononuclear-phagocytic system of young turkeys.

Macrophage cells isolated from the abdominal cavity of 21-day-old turkeys after a single injection of Sephadex suspension were used to quantitate the effects of direct in vitro exposure to deoxynivalenol (DON), 3-acetyldeoxynivalenol (3ac-DON), scirpentriol (STO), or 15-acetylscirpenol (15-MAS). Macrophage monolayers were established on glass surfaces and cells were exposed to graded levels of individual mycotoxins for 1 hour: DON, 20-640 micrograms/microliters of culture; 3ac-DON, STO, 15-MAS, 20-1280 micrograms/microliters of culture. All four mycotoxins caused dose-related effects. A concentration of 50 micrograms/microliter DON caused a significant decrease in macrophage adherence, phagocytosis of opsonized SRBC, and number of opsonized SRBC per macrophage; at 200 micrograms/microliter, phagocytosis of unopsonized SRBC was decreased. There were also increasing percentages of damaged macrophages with increasing DON doses as indicated by morphological alterations. Linear decreases in macrophage viability on exposure to 3-acDON and STO were observed. Moreover, STO and 15-MAS decreased macrophage adherence to glass and 3-acDON, STO, and 15-MAS induced macrophage morphological alterations. This study suggests that trichothecene mycotoxins may be immunosuppressive by affecting viability, adherence and phagocytic potential of mononuclear phagocytic cells of young turkeys.

Animals↗

PubMed1995

Fusarium proliferatum culture material alters several production and immune performance parameters in White Leghorn chickens.

White Leghorn Cornell K-strain chicks (3 replicates of 16 per pen) were started at Day 7 on feed amended with Fusarium proliferatum culture material containing fumonisin B1, fumonisin B2, and moniliformin at 61, 10.5, and 42.7 ppm, respectively. Observed effects on performance of treated birds included reduced feed conversion at 2 wk, and reduced body weight of males and females up to 6 wk (P < or = .05). Splenic, thymic, and liver weights, normalized for body weight, were reduced (P < or = .05) with no change in bursa of Fabricius. No significant changes were observed histologically in the spleen, bursa, kidney, heart, liver, cecal tonsils, colon, or tibia. Significant suppression in total Ig and IgG levels occurred. Macrophages from treated chicks exhibited a 34% reduction in phagocytic activity. Natural killer cell activity was not affected. These findings, which showed that Fusarium toxins alter performance and immune end points in chickens, imply that chickens exposed to mycotoxins may be more susceptible to infectious diseases.

Animals↗

PubMed1994

Effects of slaframine and 4-diphenylacetoxy-N-methylpiperidine methiodide (4DAMP) on pancreatic exocrine secretion in the bovine.

Three Holstein steers (345 +/- 22 kg) surgically fitted with a pancreatic cannula were used in two 3 x 3 Latin square design experiments to examine the effects of slaframine (SF), a muscarinic agonist, or 4-diphenylacetoxy-N-methylpiperidine methiodide (4DAMP), an M3 muscarinic glandular receptor antagonist, on pancreatic exocrine secretion. Pancreatic exocrine secretion was collected for 8 h postdosing at 30-min intervals beginning 1 h postfeeding. In experiment 1, steers were dosed with 0, 25, or 50 micrograms.kg-1 body weight (BW) of SF. Secretion of pancreatic juice and the pH of the secreted juice increased linearly (p < 0.05) with SF; however, secretion rate showed a time by treatment interaction (p < 0.05), as treatments converged 7 h postdosing. Trypsin secretion tended (p < 0.10) to show a quadratic response to SF administration, with the 25 micrograms SF.kg-1 BW dose having the lowest value. In experiment 2, steers received 50 micrograms.kg-1 BW of SF (positive control), 113 micrograms.kg-1 BW of 4DAMP (isosmolar with SF), or both. SF caused a greater pancreatic fluid secretion (p < 0.10) than 4DAMP, with SF plus 4DAMP intermediate. A time by treatment interaction (p < 0.04) was found, since treatments converged 8 h postdosing. Trypsin secretion was higher (p < 0.05) for SF than the other treatments. Chymotrypsin, alpha-amylase, and protein secretion were not affected. SF and 4DAMP alter pancreatic fluid secretion in the steer but have minimal effects on enzyme secretions.

Alkaloids↗

PubMed1993

Tropical pasture hay utilization with slaframine and cottonseed meal: ruminal characteristics and digesta passage in wethers.

Sixteen mature, ruminally cannulated wethers (average BW = 41 +/- 1 kg) were fed a low-quality hay diet with or without a cottonseed meal (CSM) supplement and the parasympathomimetic agonist slaframine (SF). Treatments were basal diet (Mitchell grass hay, 4.8% CP, 46.8% ADF) available on an ad libitum basis, basal diet plus SF (8 micrograms/kg BW, 2 x daily i.m. injection), basal diet plus CSM (41.0% CP; 100 g/d), or basal diet plus SF and CSM. Treatments were arranged as a 2 x 2 factorial within a replicated 4 x 4 Latin square with 20-d periods followed by a 10-d adjustment during which only the basal diet was fed. All measurements were performed within the final 10 d of each period. Slaframine increased salivary flow by 10 to 35% (P < .07), ruminal fluid dilution rate by 8 to 11% (P < .10), and pH by 3 to 4% (P < .001). A twofold increase (P < .05) in ruminal cellulolytic bacteria numbers occurred in SF-treated wethers. Despite these SF-induced changes in the ruminal environment, whole-tract apparent nutrient digestibility, N and mineral balance, and ruminal VFA concentrations were not changed. Cottonseed meal increased forage intake by 34 to 54% (P < .001) and DM digestibility by 30% (P < .001). Cottonseed meal supplementation of a Mitchell grass hay diet improved nutritional status and attenuated live weight loss.

Alkaloids↗

PubMed1993

Pancreatic splenic lobe organ culture system: viability and amylase release.

An organ explant culture system for the intact chick pancreatic splenic lobe (SL) was characterized for exocrine function. Organ cultures were prepared using the pancreatic splenic lobe from 9- and 15-day-old male broiler chicks (Arbor Acres x Arbor Acres) to characterize amylase release as well as tissue integrity during 2, 4, 8, and 12 h of incubation. Light microscopy studies indicated necrosis of the exocrine pancreatic acini after 4 h of incubation. Changes in islets of Langerhans were noted 4 h after incubation, but islet structural integrity remained intact for up to 12 h of incubation. Lactate dehydrogenase (LD) levels measured in the culture medium did not increase significantly from 2 to 4 h of incubation. After 4 h of incubation, total LD levels increased (P < .05) for the 9-day-old SL cultures, and LD levels increased (P < .01) per unit weight of SL for the 15-day-old cultures. Medium amylase activity did not increase after 2 h of incubation. Large increases occurred for total amylase activity and amylase activity per unit weight of SL between 4 and 12 h of incubation for both 9- and 15-day-old cultures. Histological examination as well as increases in LD and amylase activities for total and per unit weight of SL in the incubation medium suggest that the viability of the 9- and 15-day-old SL organ incubation system decreases after 4 h.

Aging↗

PubMed1992

Effect of fumonisin-B1 exposure on chicken macrophage functions in vitro.

Fumonisin-B1 (FB1) is one of the recently discovered metabolites of Fusarium moniliforme (Sheldon) occurring naturally in infected corn. It is hepatocarcinogenic and causes death in several animal species including rats, horses, swine, and ducklings. In the present study, chicken peritoneal macrophages (PM) and a chicken macrophage cell line, MQ-NCSU, were exposed in vitro to various doses of FB1. Exposure to .5, 5, and 10 micrograms FB1/mL caused significant cytotoxicity in PM after 2 and 4 h of exposure. Morphological alterations induced by FB1 in PM included cytoplasmic blebing or nuclear disintegration or both, which were maximal in cultures treated with 20 micrograms FB1/mL. Significant depression in the phagocytic potential of PM occurred after 4 h treatment with 20, 40, and 100 micrograms FB1. However, exposure to FB1 alone, as well as after stimulation with lipopolysaccharide, induced secretion of a cytolytic factor by MQ-NCSU cells. These findings, which showed that FB1 exposure induced morphological and functional alterations in chicken macrophages, imply that FB1 exposure may result in increased susceptibility of chickens to bacterial infection.

Animals↗

PubMed1990

Cholinergic manipulation of digestive function in ruminants and other domestic livestock: a review.

Exocrine secretions in the digestive tract of domestic livestock are controlled by a combination of neural and endocrine inputs. The parasympathetic domain of the autonomic nervous system is responsible for efferent signals that regulate most exocrine secretory processes. Exocrine tissues possess cholinergic muscarinic receptor subtypes that are different from those found in brain, heart and muscle tissues. Cholinergic stimulation of specific muscarinic receptor subtypes has enhanced secretions of the salivary glands and pancreas. These changes in output of exocrine glands can alter digestive function that may benefit production of cattle and swine.

Animals↗

PubMed1990

Effect of feeding diets containing corn treated with a commercial mold inhibitor (Myco Curb) on broiler-breeder performance.

Corn purchased from commercial sources was split at delivery and was left untreated or treated with a commercial mold inhibitor. Feed was prepared from these two lots of corn from within 1 wk to as much as 20 wk after delivery over the course of two experiments. There was evidence of reduced mold growth due to the mold inhibitor, particularly in the second experiment where initial mold populations were higher. Mycotoxins were evident in feed samples, regardless of the corn treatment. There was no significant effect from the treatment of corn on growth, livability, egg production, feed conversion, egg weight, or the eggshell quality of broiler breeders. Treatment of corn with a mold inhibitor significantly increased hatchability of fertile eggs in both experiments. Fertility was also significantly improved in the second experiment. These data suggest that using corn treated with a mold inhibitor results in significantly better hatchability in broiler breeders than untreated corn, although there were no observed differences in the incidence of mycotoxins in the samples taken.

Animal Feed↗

PubMed1989

Influence of dietary protein, fat or amino acids on the response of weanling swine to aflatoxin B1.

Two experiments were conducted using corn from clean or aflatoxin B1 (AFB1)-contaminated (182 ppb) sources. Weanling pigs (28 d) were fed one of eight dietary treatments arranged in a 2 x 2 x 2 factorial design. In Exp. 1 (192 pigs), treatments varied in corn source (clean or AFB1-contaminated), CP level (18 or 20%) and added fat (0 or 5%). At the end of the 28-d growth trials, plasma samples were obtained. An AFB1 x CP level interaction was detected (P less than .05) for growth rate (ADG), feed intake (FI) and feed/gain ratio (F/G). Feeding AFB1 reduced (P less than .05) ADG (.30 vs .37 kg/d) and FI (.57 vs .66 kg/d) and increased F/G (1.88 vs 1.78) of pigs fed 18% CP diets. Performance of pigs fed 20% CP diets was not altered by AFB1. Adding 5% fat to diets improved (P less than .05) F/G but did not improve ADG of pigs fed AFB1. There was an AFB1 x CP x fat interaction (P less than .05) for plasma cholesterol. Adding fat or increasing the CP level prevented the depression of plasma cholesterol in pigs fed AFB1. In Exp. 2 (96 pigs), all diets contained 18% CP and the treatments varied in corn source (clean or AFB1-contaminated), added L-lysine HCl (0 or .25%) and added DL-methionine (0 or .15%). Feeding AFB1 reduced (P less than .05) ADG of pigs fed the 18% CP diet (.44 vs .50 kg/d) but not of pigs fed diets supplemented with .25% lysine.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxin B1↗