Ppm Ochratoxin A Research Articles

Follow up long term preliminary studies on carcinogenic and toxic effects of ochratoxin A in rats and the putative protection of phenylalanine

Carcinogenic effects of ochratoxin A (OTA) on liver, kidneys, intestine, lung and eyes of Wistar rats exposed to 10 ppm or 5 ppm OTA in the diet and additionally supplemented or not with phenylalanine (PHE) were examined during 24-months experimental period. OTA was seen to provoke strong degenerative changes and slight pericapillary oedema in most internal organs, e.g. kidneys, liver, intestine, spleen and brain. Six of total nine neoplasms were identified as malignant and three as benign. Five of total six malignant neoplasms and two of total three benign neoplasms were seen in male rats. The pathological finding in rats after two weeks feeding with OTA-contaminated feed was dominated by degenerative changes in various internal organs, which were weaker in the group additionally supplemented with PHE. The protective effect of PHE was evident with respect to OTA-induced decrease of serum glucose and serum protein, but this protection was not singnificant with respect to serum enzymes activity. The number of neoplasms in PHE-supplemented group exposed to 10 ppm OTA was similar to that in the group exposed to twice lower feed levels of OTA alone, suggesting about a possible protective effect of PHE. The rats would not be able to serve as experimental model for humans with regard to OTA-induced tumorigenesis, because the target organ of OTA-toxicity in humans and pigs is mainly the kidney as opposed to the significant damages and carcinogenic effects seen in various organs in rats exposed to OTA.

Evaluation of berberine efficacy in reducing the effects of aflatoxin B1 and ochratoxin A added to male broiler rations

Many types of mycotoxins are found in food sources contaminated with fungi, and if these are ingested in large quantities or over a long period, they can affect the health of humans and domestic animals. Berberine (BBR) is a plant alkaloid with multiple pharmacological functions. This study aimed to investigate the effect of different levels of the plant alkaloid BBR on reducing toxic effects of aflatoxin B1 (AFB) and ochratoxin A (OTA) in broilers by examining performance characteristics, blood biochemistry, antioxidant systems, ileum morphology, and histopathology of the liver. The experiment was performed with 288 Ross 308 broilers reared in floor pens for 42 d in a randomized design with 9 treatments. Each treatment was replicated 4 times, and each replicate contained 8 chicks. Experimental treatments included (1) negative control diet with no additives (NC); (2) NC + 2 ppm AFB (positive control AFB; PCAFB); (3) NC + 2 ppm OTA (positive control OTA; PCOTA); (4) PCAFB + 200 mg/kg BBR; (5) PCAFB + 400 mg/kg BBR; (6) PCAFB + 600 mg/kg BBR; (7) PCOTA + 200 mg/kg BBR; (8) PCOTA + 400 mg/kg BBR; and (9) PCOTA + 600 mg/kg BBR. Compared with NC, feeding PCAFB and PCOTA diets reduced average daily feed intake, weight gain, serum concentrations of superoxide dismutase, glutathione peroxidase, and the length and width of ileum villi (P < 0.05). At the same time, these parameters increased in birds fed PCAFB or PCOTA diets supplemented with 600 mg/kg of BBR (P < 0.05). Feeding PCAFB and PCOTA diets increased feed conversion ratio (FCR), serum aspartate aminotransferase (AST), lactate dehydrogenase (LDH), alanine aminotransferase (ALT), and gamma-glutamyl transferase (GGT) activities, serum urea, and liver lesions compared with NC. By contrast, compared with PCAFB and PCOTA, adding 600 mg/kg BBR decreased FCR, AST, LDH, ALT, and GGT activities, urea, and liver lesions (P < 0.05). Overall, supplementation with 600 mg/kg BBR may improve growth performance, liver function, and antioxidant status of broilers fed diets contaminated with AFB and OTA.

Long term preliminary studies on toxic and carcinogenic effect of individual or simultaneous exposure to ochratoxin A and penicillic acid in mice

Carcinogenic effects of ochratoxin A (OTA) on liver, kidneys, intestine, muscles and subcutaneous tissue of BALB/c albino mice divided in three experimental and one control groups (30 mice in each group - 15 males and 15 females) and exposed to 10 ppm OTA and/or 50–60 ppm penicillic acid (PA) in the diet were seen. A total 22 neoplasias were found to be induced in the mice during 20 months' experimental period. Among them 14 were malignant and 8 benign. The number of neoplasias was significantly higher in the mice treated simultaneously with OTA and PA (14) compared to those in mice treated with OTA only (8). The number of malignant neoplasias was also higher (14) compared to benign neoplasias (8). Nine of a total fourteen malignant neoplasis and five of a total eight benign neoplasias were seen in the male mice. Pathological changes in mice after two weeks’ experimental period were characterized by degenerative changes in kidneys, liver and gastrointestinal tract, which were better expressed in the mice exposed simultaneously to OTA and PA. A strong synergistic effect was found between OTA and PA towards tumorogenesis. It seems that mice are not a good experimental model for humans with regard to OTA-induced tumourigenesis, because the target organ of OTA-toxicity in humans or pigs is mainly the kidney, but not the liver, intestines, subcutaneous tissue or muscles as seen in this study.

Ameliorative effect of powdered rhizome of Curcuma longa on ochratoxin A induced nephrotoxicity in broilers

A trial was conducted on broiler birds to assess the ameliorating effect of dry powdered rhizome of Curcuma longa (CL) @ 2 g/kg feed as broiler poultry feed additive against Ochratoxin A (OTA) toxicity at 0.5 ppm dietary level. Absence of clinical signs in experimental birds suggested that ochratoxicity at 0.5 ppm is subclinical in nature. Biochemical study revealed increased level of serum uric acid, urea, creatinine, sodium and potassium, indicating nephrotoxicity. Grossly, the kidneys of birds in toxicity groups showed swelling with prominent lobular pattern. Histopathologically, lining epithelial cells of tubules showed swelling, cytoplasmic acidophilia, pyknosis, narrowing of tubular lumen and detachment of tubular epithelium from basement membrane. Ultrastructural study revealed significant mitochondrial abnormality like swelling, elongation, tortuosity, ring formation and disruption of membrane. Glomeruli in toxic group showed thickened glomerular basement membrane and pyknosis in parietal epithelial cells. Use of powdered rhizome of CL significantly reduced the severity of toxicity; however, complete recovery of birds to a state comparable to control birds could not be achieved, as there was persistence of biochemical, histological and ultrastructural alterations in the birds given OTA at 0.5 ppm and supplemented with CL @ 2 g/kg feed, although the changes were of significantly mildernature compared to the birds given 0.5 ppm OTA alone. Thus, CL powder @ 2 g/kg feed could achieve partial amelioration of the toxic effect of OTA in broiler birds.

Maternal exposure to ochratoxin A targets intermediate progenitor cells of hippocampal neurogenesis in rat offspring via cholinergic signal downregulation and oxidative stress responses.

To elucidate the developmental exposure effects of ochratoxin A (OTA) on postnatal hippocampal neurogenesis, pregnant SD rats were provided a diet containing 0, 0.12, 0.6, or 3.0ppm OTA from gestation day 6 to day 21 on weaning after delivery. Offspring were maintained through postnatal day (PND) 77 without OTA exposure. At 3.0ppm, offspring of both sexes showed a transient body weight decrease after weaning. Changes in hippocampal neurogenesis-related parameters as measured in male PND 21 offspring were observed at 3.0ppm. In the subgranular zone (SGZ) of the dentate gyrus, PAX6+ or TBR2+ cells were decreased, while GFAP+ or DCX+ cells did not fluctuate in number, suggesting decreased numbers of type-2 progenitor cells. On the other hand, SGZ cells accumulating malondialdehyde increased. In the hilus of the dentate gyrus, SST+ or CHRNB2+ γ-aminobutyric acid (GABA)-ergic interneurons decreased, accompanied with transcript downregulation of Chrnb2 in the dentate gyrus. These results suggest that maternal exposure to OTA decreased type-2 progenitor cells by reducing hilar GABAergic interneurons innervating type-2 progenitor cells via cholinergic signal downregulation and also by increasing oxidative stress in the SGZ. Transcript levels of neurotrophin (Bdnf), glutamatergic receptors (Gria1, Gria2, and Grin2a), serotonin-synthesizing enzyme, and serotonergic receptors (Tph2, Htr1a, and Htr4) increased in the dentate gyrus, suggesting multiple neuroprotective actions against OTA-induced aberrant neurogenesis. All observed fluctuations were reversed by PND 77. The no-observed-adverse-effect level for offspring neurogenesis was determined to be 0.6ppm, corresponding to 39.3-76.0μg/kg body weight/day.

Pathology of Ochratoxin A–Induced Nephrotoxicity in Japanese Quail and Its Protection by Sea Buckthorn (Hippophae rhamnoidesL.)

The present study was designed to study the protective effect of sea buckthorn (SBT) against renal damage induced by ochratoxin A (OTA) in Japanese quail. Day-old quail chicks were divided into six groups and fed a basal quail chick mash containing 2% SBT leaf powder (group SX), OTA at a dietary level of 3 ppm (group OX), 25 ppm L-beta-phenylalanine (Phe) plus 3 ppm OTA (group OP), 2% dietary level of SBT leaf powder plus 3 ppm OTA (group OS), SBT leaf extract at a level of 10%/L of drinking water plus 3 ppm OTA (group OSS), and a standard toxin-free feed (group CX, control) for 21 days. OTA at 3 ppm level in diet grossly revealed mild to moderate renal swelling in OX birds, and the severity was less in the case of OS, OSS, and OP birds. Microscopically, degenerative, necrotic, and inflammatory changes were observed in OX birds, but the changes were less severe in OS, OSS, and OP birds. Ultrastructural studies revealed remarkable and consistent changes in the proximal convoluted tubules (PCTs), with severe damage of mitochondria and endoplasmic reticulum in OX birds, whereas SBT-treated birds (groups OS, OSS) had mild changes in mitochondria. A moderate to marked increase in number of peroxisomes in the cytoplasm of PCTs was a consistent finding in the Phe- and SBT-treated groups kept on OTA in comparison to the group fed OTA alone. In conclusion, the inclusion of 2% SBT leaf powder in feed and SBT leaf extract in water provided partial protection against OTA-induced nephropathy in Japanese quail.

Histopathological changes in the kidneys of Japanese quail associated with fumonisin B1 and ochratoxin A in feed

This study describes the toxic interaction of fumonisin B1 (FB1) and ochratoxin A (OTA), alone and in combination for histopathological changes of the kidneys in day-old Japanese quail. Quail chicks were divided into four groups and fed with basal quail chick mash containing FB1 at 200 ppm (group FX), OTA at 2 ppm (group OX), and FB1 at 200 ppm+OTA at 2 ppm (group FO) and standard toxin- free feed (group CX, control) for 28 days. Results of the present study showed that feeding of diets amended with 200 ppm FB1 and 2 ppm OTA led to mild to moderate swelling of the kidneys in a few birds fed FB1. However, swelling in the kidneys of the group fed OTA alone revealed mild to severe swelling with occasional dilatation of the ureters. The kidneys revealed swelling of tubular epithelial cells, presence of eosinophilic proteinaceous material in tubular lumen, and tubular epithelial cells in FB1 fed group, while mainly, swelling of proximal convoluted tubule epi- thelial cells with indentation of nuclear membranes was a conspicuous finding noticed in OTA and combination treat- ment groups.

Isolation, screening and identification of Swine gut microbiota with ochratoxin a biodegradation ability.

The potential for ochratoxin A (OTA) degradation by swine intestinal microbiota was assessed in the current study. Intestinal content that was collected aseptically from swine was spiked with 100 ppb OTA and incubated for 6 and 12 h at 39°C. An OTA assay was conducted using the incubated samples, and it was found that 20% of the OTA toxin was detoxified, indicating the presence of microbes capable of OTA degradation. Twenty-eight bacterial species were isolated anaerobically in M 98-5 media and 45 bacterial species were isolated using nutrient broth aerobically. Screening results showed that one anaerobic bacterial isolate, named MM11, detoxified more than 75% of OTA in liquid media. Furthermore, 1.0 ppm OTA was degraded completely after 24 h incubation on a solid ‘corn’ substrate. The bacterium was identified by 16S rDNA sequencing as having 97% sequence similarity with Eubacterium biforme. The isolation of an OTA-degrading bacterium from the swine natural flora is of great importance for OTA biodegradation and may be a valuable potential source for OTA-degradation enzymes in industrial applications.

Studies on carcinogenic and toxic effects of ochratoxin A in chicks.

Carcinogenic/toxic effects of ochratoxin A (OTA) in various internal organs of Plymouth Rock chicks were determined. The number of OTA-induced neoplasms was similar in chicks given 25 ppm L-β-phenylalanine (PHE) in addition to 5 ppm OTA compared to chicks given only 5 ppm OTA, which showed that PHE cannot be used as a real protector against the carcinogenic or toxic effects of OTA in chicks. OTA was found to provoke strong degenerative changes in liver and kidneys, degenerative changes and depletion of cells in lymphoid organs, oedematous and degenerative changes in the brain, muscular haemorrhages and fatty changes in the bone marrow. The target organs for carcinogenic effect of OTA in chicks were found to be kidneys and liver.

Effect of Saccharomyces cerevisiae and esterified glucomannan on residues of Ochratoxin A in kidney, muscle and blood of laying hens

The in vivo capability of Saccharomyces cerevisiae (SC), and of an esterified glucomannan (EGM) to reduce the oral bioavailability of ochratoxin A (OTA) added to a basal diet for laying hens was checked over a 12 week period. The residues of OTA in kidney, muscle and blood were studied. Eighty-four Isa Brown laying hens were divided into 6 experimental groups, fed 6 different diets: 0-0: basal diet; EGM-0: diet supplemented with 0.2% EGM; SC-0: diet supplemented with 0.2% SC; 0-OTA: diet supplemented with 0.2 ppm OTA; EGM-OTA: diet supplemented with 0.2% EGM and 0.2 ppm OTA; SC-OTA: diet supplemented with 0.2% SC and 0.2 ppm OTA. During the trial feed and water were provided ad libitum and all the animals were clinically observed. At the end of the experimental period and immediately before the hens were euthanized, blood samples were collected; kidneys, and muscle were sampled. The ochratoxin A was checked using a HPLC flourometric method. During the trial all the hens were healthy. All the biological matrices of the OTA administered hens were positive to the mycotoxin; the recorded levels were very low and decreased in the order: kidneys < blood < muscle.

Effect of ochratoxin A on broiler chicks challenged with Salmonella gallinarum

1. A study was conducted to evaluate the effects of ochratoxin A (OA) on broiler chicks challenged with Salmonella gallinarum. 2. One hundred and seventy-six 1-d-old broiler chicks were divided into two groups of 88 chicks each, with one group fed on a control mash diet and the other given a mash diet containing 2 ppm OA. On d 14, each group was further subdivided into two groups with one group infected with S. gallinarum and the other uninfected. 3. Following S. gallinarum inoculation on d 14, 4 birds from each group were killed at 1, 2, 3, 5, 7, 10, 14 and 21 d post inoculation. 4. S. gallinarum infection caused dullness, depression, weakness, increased thirst, droopy wings, ruffled feathers and greenish-yellow diarrhoea. S. gallinarum infection in the absence of OA caused 11·5% mortality which increased to 28·8% in the presence of OA. 5. Decreased body weight and reduced feed intake were observed in chicks fed on the diet containing OA. S. gallinarum infection also reduced the body weights of chicks, with the effects being more marked in chicks receiving OA. The OA diet led to increased serum levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, uric acid and creatinine, and decreased levels of total proteins, albumin, globulins, calcium and phosphorus. S. gallinarum infection did not cause significant alteration in any of the serum biochemical parameters. 6. Mortality and the severity of S. gallinarum infection in broiler chicks were increased by the presence of OA in the diet.

Effects of exposure time and dietary ochratoxin A level on broiler performance

The present study was designed to examine the harmful effects of low level ochratoxin A (OTA) for different period and different dietary OTA levels for same period of ingestion as well as to assess the resting period necessary to revoke any adverse effects of OTA. The trial was performed on 72 day-old chickens with 12 broilers in each group. The experimental groups were offered feed contaminated with 0.5 ppm OA during 7, 14 or 21 days in the first evaluation, and feed contaminated with 0.5, 1.0 or 1.5 ppm OTA for 7 days in the second evaluation. The control group (K) received feed free of toxin. Broilers in the control groups had an average daily gain of 43.5 g and a feed: gain ratio of 1.97 kg. OTA expressed a negative effect on performance proportion to the time of exposure and to the amount of dietary toxin showing prolong and cumulative effects. Early detection of OTA and exclusion of contaminated feed could partially prevent its adverse effects, but not less than three weeks of recovery is needed to nullify the damage.

The effect of high and low doses of ochratoxin A in feed on growing chicken

Effects of high and low dose of ochratoxin A (OTA) as pure toxin supplemented to feed were investigated on the performance of growing chicken. Two groups were fed with different doses of chemical pure OTA 0.5 ppm and 5 ppm in feed and the effects of toxin on body and organ weights were studied and compared with control group. No effects were observed by feeding 0.5 ppm OTA, whereas 5 ppm had a negative effect on the daily body mass gain. OTA in feed had a negative effect on the daily body mass gain. In contrary nephrotoxic effects could be observed by feeding the naturally OTA contaminated feed with only 0.2 ppm of OTA produced byPenicillium verrucosum.

Beneficial effects of dietary ascorbic acid supplement on hens subjected to ochratoxin A toxicosis under normal and high ambient temperatures

Three experiments were conducted to study ochratoxin A (OA) toxicity and the effect of supplemental ascorbic acid (AA) in laying hens housed under two environmental temperatures. In exp. 1, 18 hens were divided into three groups of six hens and fed diets containing either 0, 1.7, or 3.1 ppm OA for 14 d. In exps. 2 and 3, 24 hens were randomly assigned to four dietary treatments in six replications. Treatments consisted of a control and three diets containing either 300 ppm AA, 3 ppm OA, or 300 ppm AA plus 3 ppm OA. Treatment diets were fed for 14 d following the feeding of the basal diet for 14 d. The test-period temperature was 25 °C in exp. 1 and 2 and 33 °C in exp. 3. In exp. 1, feeding OA at 1.7 ppm significantly (P ≤ 0.05) decreased feed intake and increased liver weights and eggshell elasticity. At 3 ppm, OA significantly (P ≤ 0.05) reduced feed intake, body-weight change and egg production, and increased shell elasticity. Similar trends were also observed in exps. 2 and 3 when laying hens were fed 3 ppm OA compared with those fed the control diet. An analysis of plasma constituents showed that OA also increased Cl− concentration and aspartate transaminase activity and decreased plasma Ca++ concentrations. Exposing hens to 33 °C (compared with 25 °C) appeared to aggravate the negative effects of OA. All the negative effects of OA, apart from body-weight changes, reductions in feed intake, and increases in eggshell elasticity at 33 °C, were either moderated or significantly (P ≤ 0.05) reversed by dietary AA supplementation. The results suggest that some of the detrimental effects of OA in the diet of the laying hen can be counteracted by dietary supplementation of AA. Key words: Ochratoxin A, toxicity, ascorbic acid, hen, temperature

Characterization of the Toxicity of the Mycotoxins Aflatoxin, Ochratoxin, and T-2 Toxin in Game Birds. I. Chukar Partridge

Chukar partridges were fed diets containing 1.25, 2.5, or 5 ppm aflatoxin; 1, 2, or 4 ppm ochratoxin A (OA); or 4, 8, or 16 ppm T-2 toxin. Toxin-induced mortality was seen during the third week with 4 ppm OA (12.5%) and 16 ppm T-2 toxin (15%), compared with the mortality in control chukars fed no toxin (2.5%). Body weights were significantly decreased by the highest level of aflatoxin at 3 weeks of age, by the highest level of OA by 2 weeks of age, and by 8 and 16 ppm T-2 toxin by 1 week of age. Aflatoxin did not affect liver weight and OA did not increase kidney weight in 3-week-old chukars. There was a slight decrease in kidney weight in chukars fed 4 ppm OA; however, the decrease was related to the decrease in body weight produced by the toxin. Mouth lesions were seen at all levels of T-2 toxin fed.

COMPARISON OF THE EFFECTS OF TOXIN-FREE AND TOXIN-CONTAINING MOLD-CONTAMINATED BARLEY ON CHICK PERFORMANCE

Three chick (Single Comb White: Leghorn) growth trials were conducted using chemically characterized, toxin-free mold-contaminated barley samples naturally contaminated with Penicillium cyclopium and Aspergillus flavus fungi. The concentrations of fungal (mold) material in the samples, estimated by chemical analysis, ranged from about 1 to 16%. Compared to a mold-free barley control, the mold-contaminated barleys were generally higher in percent protein, ash and ADF, but had much lower bushel weights and percent fat and starch. The first trial compared the effects of feeding mold-free barley and 30% (wt/wt) of the 16% mold-contaminated barley in combination with 0, 2 and 4 ppm ochratoxin A (OA) on chick performance and nutrient digestion. Relative to controls, the average decreases in feed consumption (RFC) and weight gain (RWG) for birds fed the mold-contaminated barley were 50 and 80%, respectively. In contrast, 4 ppm of OA caused corresponding reductions of 22 and 30%, while in combination, mold and OA reduced performance slightly more than the mold alone. Similarly, apparent dry matter (DM), fat and protein digestibilities for birds fed mold-contaminated barley decreased 16.7, 37.7 and 13.7, respectively, compared to controls, but only 10.7, 21.5 and 12.0% for those fed 4 ppm OA. A second trial compared mold-contaminated barley samples from different sources with different degrees of contamination. Decreases in RFC and RWG were directly related (R2 = 0.96) to the mold concentration of the diet. The final study examined the effect on chick performance of incorporating increasing dietary concentrations of heavily contaminated (16% mold) mold-contaminated barley. As in trial 1, RFC and RWG were markedly affected by increasing dietary mold-contaminated barley. For example, the presence of only 15% (wt/wt) of the heavily contaminated mold-contaminated barley in the diet caused reductions of 20 and 30% in RFC and RWG, respectively. Apparent DM, fat and protein digestibilities again were all significantly (P &lt; 0.0001) reduced by the mold. The results indicate the mold-contaminated barley can have a serious detrimental effect on chick performance, even when no toxins are detectable. Nutrient digestibility data suggest that antinutritive agent(s) in the mold-contaminated barley act to impair utilization of dietary nutrients rather than only those of the affected barley. Factors affecting diet palatability may also be involved. Key words: Mold, toxin-free, mycotoxin, ochratoxin A, barley, chick performance, apparent nutrient digestibility

Effect of ochratoxin A on immunoglobulins in broiler chicks

The effect of ochratoxin A (OA) on the immune system was investigated in broiler chicks fed graded dietary levels of OA up to 4 ppm for 20 days from hatch. Immunofluorescent demonstration of IgG, IgA and IgM in sections of liver, kidney and lymphoid tissues was used to assess immune competence. Serum immunoglobulin levels were measured by radial immunodiffusion. Ochratoxin caused a significant depression in immunoglobulin-containing cells in all the lymphoid organs studied. Correspondingly, total immunoglobulin levels were also reduced in the sera from OA fed birds, immunosuppression being similar at both the 2 and 4 ppm OA levels. Deposition of immunoglobulins, especially IgG, in the glomerular basement membrane was seen with greater frequency in kidneys from OA fed fowls. Immunoglobulin-containing lymphoid cells occurred more frequently in the kidney parenchyma of these birds.

Toxicity of Ochratoxin A and Tannic Acid to Growing Chicks

The effects of ochratoxin A (OA) and tannic acid (TA) on growing chicks were determined. One-day-old male broiler chicks were fed a diet containing the following additives for 26 days: A) none; B) 3.0 ppm OA; C) 1.5% TA; D) 3.0 ppm OA plus 1.5% TA. When compared to the controls, body weights and feed efficiencies were significantly depressed in the OA and TA groups. There was a further depression in body weights and a dramatic depression of feed efficiency in the OA-TA combination group. Pigmentation, as measured by visual shank scores, was reduced in chicks fed OA singly or in combination with TA but was not affected by feeding TA singly. There were no consistent treatment differences in the relative weights of the kidney, gizzard, proventriculus, liver, bursa, or pancreas, although there was a trend toward an elevated relative kidney weight in the groups receiving OA. Serum uric acid levels were significantly elevated in the OA and the OA-TA combination group indicating impaired renal excretory function attributable to OA. Total serum protein levels were significantly depressed in the groups receiving OA, and serum calcium levels were depressed in all treatment groups. Serum phosphorus levels were decreased in the OA and OA-TA groups but were only decreased significantly in the OA group. There were no consistent treatment differences in the hematology and other blood chemistry and mineral values.

Effects of Ochratoxin A on Egg Production, Body Weight, and Feed Intake in White Leghorn Hens

Two trials were conducted to determine whether ochratoxin A (OA) or reduced feed consumption was responsible for reduced body weight and egg production in hens. In an 8 week restricted feed intake trial two groups of White Leghorn hens received amounts of non-contaminated feed similar to that consumed in a previous trial by hens fed either noncontaminated diet or one containing 4 ppm OA. A significant (P<.05) loss of body weight was observed during the 5th and 6th weeks in the group receiving a similar amount of feed as the OA-treated group in the previous trial, indicating that reduced feed consumption might account for the loss in body weight. Since egg production was not affected, it was possible that OA may depress egg production through a mechanism that is separate from its influence on feed intake. In an organoleptic trial White Leghorn hens were offered a choice of layer feed either with or without OA added for a three week period. There was a significant (P<.05) reduction in the consumption of OA-contaminated feed.

Effects of Ochratoxin A on Growth Response and Residues in Broilers

The effects of continuous feeding of graded levels (.5, 1.0, 2.0 ppm) of ochratoxin A (OA) for eight weeks to male and female broiler chickens were investigated. A depression in body weight gain was observed in all groups receiving OA. The depression was proportional to the level of exposure to OA and was more marked and prolonged in males than in females. Detectable residues of OA were observed in the liver and kidney of birds fed 2 ppm OA. Residues disappeared from liver within 24 hr and from kidney within 48 hr after withdrawal of the mycotoxin from feed. No residues of OA were found in muscle or fat.