Biological suppression of aflatoxicosis in Japanese quail (Coturnix coturnix japonica) by dietary addition of yeast (Saccharomyces cerevisiae).

The amelioration of aflatoxicosis in Japanese quails was examined by the dietary addition of live yeast (Saccharomyces cerevisiae; SCE). Yeast incorporated into the diet at 1 g kg(-1) was evaluated for its ability to reduce the deleterious effects of 2.5 mg total aflatoxin (AF; 82.30 per cent AFB1, 2.06 per cent AFB2, 7.68 per cent AFG1 and 7.96 per cent AFG2) kg(-1)diet on growing Japanese quail chicks from 10 days to 45 days of age. Forty 10-day-old Japanese quail chicks were assigned to 2x2 factorial arrangement of treatments (control, AF, SCE, AF plus SCE) each consisting of 10 quails. The performances of birds were evaluated. The AF treatment significantly and dramatically decreased food consumption and body-weight gain from the first week onwards. The significant adverse effect of AF on the food conversion ratio was also determined from week 1 to the end of the experiments. The addition of SCE to the AF -containing diet significantly reduced these deleterious effects of AF on food consumption, body-weight gain and food conversion ratio. Compared to controls, the cumulative body weight gain was reduced by 37 per cent among the quails consuming AF without SCE, but increased 15 per cent for the birds fed AF plus SCE. Interestingly, the single inclusion of SCE to the AF-free diet provided significant improvements in all the investigated growth performances of birds (approximately 40 per cent) compared to controls.     

Aflatoxicosis in Iowa swine: eight cases (1983-1985)

During 1983, 1984, and 1985, aflatoxicosis was diagnosed in 8 Iowa swine herds after the herds were fed corn from the 1983 corn crop. As a result of the diagnosis, the associated environmental conditions, clinical signs of aflatoxicosis, macroscopic and microscopic lesions, aflatoxin concentrations detected in feeds, and management of affected swine were reviewed. Concentrations of aflatoxin in shelled corn and complete feed were as high as 2,020 ng and 1,200 ng of aflatoxin (B1 and B2)/g of feed, respectively. Clinical signs of aflatoxicosis included decreased feed consumption and weight loss. Some pigs died acutely, but death often was preceded by a period of clinical disease. Greater morbidity and mortality were observed in swine herds that consumed greater concentrations of aflatoxin.     

Characterization of the toxicity of the mycotoxins aflatoxin, ochratoxin, and T-2 toxin in game birds. III. Bobwhite and Japanese quail.

Bobwhite and Japanese quail were fed diets containing 1.25, 2.50, or 5.00 ppm aflatoxin; 1, 2, or 4 ppm ochratoxin A (OA); or 4, 8, or 16 ppm T-2 toxin. Aflatoxin induced mortality in bobwhites during the second and third week with 1.25 ppm (10%), 2.50 ppm (30%), and 5.00 ppm (40%), and during the same period with T-2 toxin at 8 ppm (20%) and 16 ppm (22.5%). Body weights of bobwhite quail were significantly decreased by the two higher levels of aflatoxin by 2 weeks of age, and by the two higher levels of T-2 toxin by 1 week of age. In Japanese quail, only the highest level of aflatoxin and T-2 toxin reduced body weight (by 3 weeks and by 1 week of age, respectively), and even then to a much lesser extent than in bobwhites (less than 10%). Aflatoxin did not affect feed-conversion ratio (FCR) in bobwhite quail, but the two higher levels of T-2 toxin increased FCR. None of the toxins induced mortality or increased the FCR in Japanese quail. Aflatoxin increased liver weight in both bobwhite and Japanese quail. OA increased kidney weight in 3-week-old Japanese quail but had no effect on the kidney weight of bobwhite quail. Mouth lesions were progressively more severe in bobwhite quail fed increasing levels of T-2 toxin, but lesions were far less severe in Japanese quail.     

Biological suppression of aflatoxicosis in Japanese quail (Coturnix coturnix japonica) by dietary addition of yeast (Saccharomyces cerevisiae)

The amelioration of aflatoxicosis in Japanese quails was examined by the dietary addition of live yeast (Saccharomyces cerevisiae; SCE). Yeast incorporated into the diet at 1 g kg⁻¹was evaluated for its ability to reduce the deleterious effects of 2·5 mg total aflatoxin ( ; 82·30 per cent ₁ , 2·06 per cent ₂, 7·68 per cent ₁and 7·96 per cent ₂) kg⁻¹diet on growing Japanese quail chicks from 10 days to 45 days of age. Forty 10-day-old Japanese quail chicks were assigned to 2×2 factorial arrangement of treatments (control, , , plus ) each consisting of 10 quails. The performances of birds were evaluated. The treatment significantly and dramatically decreased food consumption and body-weight gain from the first week onwards. The significant adverse effect of on the food conversion ratio was also determined from week 1 to the end of the experiments. The addition of to the -containing diet significantly reduced these deleterious effects of on food consumption, body-weight gain and food conversion ratio. Compared to controls, the cumulative body weight gain was reduced by 37 per cent among the quails consuming without , but increased 15 per cent for the birds fed plus . Interestingly, the single inclusion of to the -free diet provided significant improvements in all the investigated growth performances of birds (approximately 40 per cent) compared to controls.     

Effect of coccidiosis on reproductive maturation of male Japanese quail

The effects of coccidiosis on reproductive development of male Japanese quail were examined. Male Japanese quail were exposed to high (5 x 10(5) sporulated oocysts/quail) or low (5 x 10(3) sporulated oocysts/quail) doses of Eimeria uzura at 16 or 30 days of age and sampled at 37 days. Quail given high doses of coccidia had reduced testes weight and lowered circulating concentrations of androgen compared with control males. Low doses of coccidia did not affect testes weight but did result in elevated plasma androgen levels. There were no differences in average testes weights by 51 days; however, plasma androgen was still reduced in most groups. To study the effects of coccidiosis on egg production, males exposed to high doses of coccidia at 16 (16H) or 30 (30H) days of age were mated with control females, and control males were mated with control or 16H females. The onset of laying was delayed for 5 days in the control male: 16H female group. During the first week of production, eggs from females bred to 30H males had lower fertility and hatchability than those bred to control or 16H males. By the third week of production, levels of fertility were similar. Apparently, exposure of quails to coccidiosis before sexual maturation might result in long-term effects on later reproductive capability.     

Aflatoxicosis in nine dogs after exposure to contaminated commercial dog food.

The purpose of this study was to characterize light and electron microscopic findings from 9 dogs that had consumed aflatoxin-contaminated commercial dog food from recalled batches. Four dogs died and 5 were euthanized after signs of liver failure. Analysis of feed and liver samples confirmed exposure to aflatoxin. Of the 9 dogs, 8 had classic signs of liver failure, and 1 had signs of liver failure. Enlarged, pale yellow livers were seen macroscopically at necropsy in the dogs with subacute hepatopathy, and cirrhosis was noted in the dog with chronic hepatopathy. Histopathologic findings included hepatic lipidosis, portal fibroplasia, and biliary hyperplasia, which supported a diagnosis of subacute toxic hepatopathy in the 8 symptomatic animals. Marked lobular atrophy, bridging portal fibrosis, and regenerative hepatocellular nodules characterized the dog with chronic hepatopathy. Electron microscopy revealed marked hepatocellular lipid vacuolation and early fibroplasia in the dogs with acute hepatopathy and marked fibrosis and regeneration in the dog with chronic hepatopathy. Analysis of feed for aflatoxin consistently revealed high levels of aflatoxin B1 (range of 223-579 ppb), and hepatic tissue contained elevated levels of aflatoxin B1 metabolite M1 (0.6-4.4 ppb). Although dogs are not commonly affected by aflatoxicosis, they are highly susceptible and can present with classic signs of acute or chronic hepatopathy. Characteristic gross, histologic, and electron microscopic changes help pathologists determine a presumptive toxic insult. Detecting aflatoxins or their metabolites in feed or liver specimens can help confirm the diagnosis of aflatoxicosis.     

Effects of aflatoxin ingestion on the development of Moraxella bovis infectious bovine keratoconjunctivitis

A study was conducted to determine whether measured doses of aflatoxin given under different schedules would influence the pathogenesis of Moraxella bovis induced infectious bovine keratoconjunctivitis (IBK). Calves were allotted to 4 groups (groups I-IV) of 9, 9, 9, and 8 calves, respectively. Group I calves were given aflatoxin for 11 consecutive days starting 5 days before their eyes were exposed to M. bovis. Group II calves were given aflatoxin for 5 consecutive days starting 7 days after their eyes were exposed to M. bovis. Group III calves were given aflatoxin for 5 consecutive days starting 21 days after their eyes were exposed to M. bovis. Group IV calves were not given aflatoxin; but their eyes were exposed to M. bovis on the same day as were the eyes of calves in groups I-III; these calves served as controls. Aflatoxin had little if any influence on the pathogenesis of IBK under the conditions of this study. The results did not rule out an exacerbating effect of M bovis infection on aflatoxicosis in calves. Calves with the highest concentration of aflatoxin in their blood had the more severe signs of aflatoxicosis. Possible reasons for the equivocal results are discussed.     

Major biological consequences of aflatoxicosis in animal production.

Aflatoxins, a family of closely related, biologically active mycotoxins, have been known as a prominent cause of animal disease for 30 yr. The toxins occur naturally on several key animal feeds, including corn, cottonseed, and peanuts. Occurrence of aflatoxin on some field crops tends to spike in years when drought and insect damage facilitate invasion by the causative organisms, Aspergillus flavus and A. parasiticus, which abound in the crop's environment. Acute aflatoxicosis causes a distinct overt clinical disease marked by hepatitis, icterus, hemorrhage, and death. More chronic aflatoxin poisoning produces very protean signs that may not be clinically obvious; reduced rate of gain in young animals is a sensitive clinical register of chronic aflatoxicosis. The immune system is also sensitive to aflatoxin, and suppression of cell-mediated immune responsiveness, reduced phagocytosis, and depressed complement and interferon production are produced. Acquired immunity from vaccination programs may be substantially suppressed in some disease models. In such cases the signs of disease observed are those of the infectious process rather than those of the aflatoxin that predisposed the animal to infection. Mixtures of aflatoxin with other mycotoxins can result in greatly augmented biological responses in terms of rate of gain, lethality, and immune reactivity. Because of its great biological activity, its wide-spread potential presence in areas where critical feed crops are grown, and its propensity to spike in problem years, aflatoxin promises to be a continuing problem in animal production.     

Aflatoxicosis in feedlot cattle

Aflatoxicosis was diagnosed in lightweight feedlot cattle fed aflatoxin-contaminated cottonseed or gin trash. Clinical signs of hepatic damage and death were recorded for more than 200 of the 14,000 animals in a feedlot. Aflatoxin concentration in feedlot products fed to these cattle ranged from 96 to 1,700 ng/g. Diagnosis was based on the correlation of characteristic microscopic liver lesions, high concentration of aflatoxin in cottonseed feed products, and isolation and detection of aflatoxin B1 and aflatoxin M1 in urine and liver from affected calves. This report describes a large-scale outbreak of aflatoxicosis and demonstrates the need for careful quality control of feed products susceptible to aflatoxin contamination.     

Protective effect of L-carnitine against oxidative damage caused by experimental chronic aflatoxicosis in quail (Coturnix coturnix)

This study was designed to evaluate the effect of L-carnitine supplementation on the plasma malondialdehyde (MDA) and whole blood reduced glutathione (GSH) concentrations in experimentally-induced chronic aflatoxicosis in quails. For this purpose, a total of 80 quails up to 8 weeks old were divided into four equal groups. Group I served as control, Group II was given L-carnitine at the dose of 200 mg/litre in the drinking water for 60 days, Group III was given 60 microg total aflatoxin/kg diet for 60 days, and Group IV was given both 60 microg total aflatoxin/kg diet and 200 mg L-carnitine/litre in the drinking water for 60 days. Aflatoxin treatment caused a significant increase in plasma MDA and a significant decrease in blood GSH concentrations. On the other hand, there was a significant decrease in plasma MDA and a significant increase in whole blood GSH in the L-carnitine-supplemented group. The present study demonstrated that L-carnitine brought about the inhibition of lipid peroxidation by enhancing antioxidant capacity in quails with chronic aflatoxicosis.     

The effect of high doses of aflatoxin on the pig]

In two experiments, 18 pigs were given feed contaminated with aflatoxin which had been prepared by the extraction of the cultures of toxinogenic strains of the fungus Aspergillus flavus. After the ingestion of aflatoxin (AFB1) at a dose of 5.4 to 10.5 mg per kg of live weight, the pigs showed symptoms of peracute aflatoxicosis and died within 12--20 hours. After ingestion of AFB1 at a dose of 1.4 or 3.1 mg per kg live weight, the pigs suffered from acute aflatoxicosis and died within 3 to 26 days from the administration of the contaminated feed. In the cases of these experimental aflatoxicoses, clinical symptoms, haematological and biochemical changes in the blood and the patho-anatomical and histological findings in the swine organism were described.     

Clinical and clinicopathologic features of dogs that consumed foodborne hepatotoxic aflatoxins: 72 cases (2005-2006)

OBJECTIVE: To characterize clinical signs, clinicopathologic features, treatments, and survival in dogs with naturally acquired foodborne aflatoxicosis. DESIGN: Retrospective case series. ANIMALS: 72 dogs that consumed aflatoxin-contaminated commercial dog food. PROCEDURES: Medical records of affected dogs were reviewed. Between December 2005 and March 2006, dogs were identified as having foodborne aflatoxin hepatotoxicosis on the basis of the history of consumption of contaminated food or characteristic histopathologic lesions (subject dog or a recently deceased dog in the same household or kennel). Recorded information included signalment, clinical features, clinicopathologic test results, treatments, and survival. Data were analyzed by survival status. RESULTS: Most dogs were of large breeds from breeding kennels. No significant differences were found in age or weight between 26 (36%) survivor dogs and 46 (64%) nonsurvivor dogs. Severity of clinical signs varied widely; 7 dogs died abruptly. In order of onset, clinical features included anorexia, lethargy, vomiting, jaundice, diarrhea (melena, hematochezia), abdominal effusion, peripheral edema, and terminal encephalopathy and hemorrhagic diathesis. Common clinicopathologic features included coagulopathic and electrolyte disturbances, hypoproteinemia, increased serum liver enzyme activities, hyperbilirubinemia, and hypocholesterolemia. Cytologic hepatocellular lipid vacuolation was confirmed in 11 dogs examined. In comparisons of clinicopathologic test results between survivor and nonsurvivor dogs, only granular cylindruria (7/21 dogs) consistently predicted death. Best early markers of aflatoxicosis were low plasma activities of anticoagulant proteins (protein C, antithrombin) and hypocholesterolemia. Despite aggressive treatment, many but not all severely affected dogs died. CONCLUSIONS AND CLINICAL RELEVANCE: Serum liver enzyme activities and bilirubin concentration were unreliable early markers of aflatoxin hepatotoxicosis in dogs. Hypocholesterolemia and decreased plasma protein C and antithrombin activities may function as exposure biomarkers.     

Susceptibility of various poultry species to dietary aflatoxin

1. The relative sensitivities of broiler chicks, White Leghorn chicks, quail chicks, goslings and turkey poults to increasing dietary contents of aflatoxin from 1 to 21 d of age were determined. Aflatoxin was included in the diets at three concentrations (0.7, 1.4 and 2.1 mg aflatoxin B_a equivalents /kg).

2. Data were analysed for species differences in food consumption, body weight, food utilisation, mortality and liver pathology.

3. There were no significant effects of aflatoxin in broiler and Leghorn chicks. Aflatoxin at 0.7 mg/kg decreased the body weight of turkey poults but tended to increase the growth rate of goslings. At 1 ‐4 mg aflatoxin/kg food consumption, body weight and weight gain of goslings were adversely affected.

4. Liver damage occurred in goslings and quail chicks at all inclusions of aflatoxin and was extensive at 2.1 mg/kg.

5. Poults and goslings appeared to be the most sensitive, quail were intermediate and domestic chicks were most resistant.     

Effect of clinoptilolite on performance of Japanese quail (Coturnix coturnix japonica) during experimental aflatoxicosis

Clinoptilolite (CLI, a natural zeolite), incorporated into the diet at 50 g/kg, was evaluated for its ability to reduce the deleterious effects of 2.0 mg total aflatoxin (AF;83.06% AFB1, 12.98% AFB2, 2.84% AFG1 and 1.12% AFG2)/kg diet on growing Japanese quail chicks from 10 to 45 d of age. A total of 40 Japanese quail chicks were divided into 4 treatment groups (control, AF, CLI, AF plus CLI) each consisting of 10 chicks. The performance of the birds was evaluated. The AF treatment significantly decreased food consumption and body weight gain from the 3rd week onwards. The adverse effect of AF on food conversion ratio was also significant from week 4 of the experiment. The addition of CLI to an AF-containing diet significantly reduced the deleterious effects of AF on food consumption, body weight gain and food conversion ratio. Food consumption was reduced by 14% in quail chicks consuming the AF diet without CLI, but by only 6% for quail chicks consuming the AF plus CLI diet. Similarly, overall body weight gain was reduced by 27% in birds consuming the AF diet without CLI, but by only 8% for birds consuming the AF plus CLI diet. The addition of CLI to the AF-free diet significantly decreased food consumption and body weight gain during week 4, but these parameters were similar to the controls in week 5. No mortality was observed in any of the groups. These results suggest that CLI effectively diminished the detrimental effects of AF on the variables investigated in this study.     

MC1R基因与朝鲜鹌鹑羽色关系的研究

黑素皮质素受体1(MC1R)又称促黑素细胞激素受体(MSH-R),由毛色扩展位点编码而成,对动物体色的形成起重要作用,本研究分析了MC1R基因突变与朝鲜鹌鹑羽色之间的关系。通过混合样品DNA测序方法寻找MC1R基因的突变位点,采用PCR-SSCP的方法对突变位点在4种羽色鹌鹑(栗羽、黄羽、白羽、黑羽)群体中的分布情况进行了研究,以揭示MC1R基因与鹌鹑羽色性状之间的关系。结果表明,在鹌鹑MC1R基因上存在一个A/G突变位点,导致编码蛋白发生Ile58Val突变,通过PCR-SSCP分析发现,该突变位点在4种羽色鹌鹑群体间没有显著差异(P>0.05)。本研究没有发现与日本鹌鹑报道相同的Glu92Lys突变位点,表明朝鲜鹌鹑的黑羽突变与报道的日本鹌鹑黑羽突变的机制不同,而且朝鲜鹌鹑的黑羽突变可能还与其它基因突变有关。     

Effects of various treatments on induced chronic aflatoxicosis in rabbits

Male New Zealand White rabbits were orally given 0.05 mg of aflatoxin B1 (AFB1)/kg of body weight daily for 10 days and were treated with glutathione-precursors and depletor, antibacterial agents, or sodium thiosulfate. The drug administered, the mortality, and the mean survival time were as follows: corn-oil controls (0), euthanatized at 25 days; AFB1-controls (2), 21 days; AFB1 and saline controls (2), 22 days; cysteine and AFB1 (5), 13 days; methionine and AFB1 (5), 12 days; sodium thiosulfate and AFB1 (2), 21 days; sulfadimethoxine and AFB1 (1), 24 days; oxytetracycline and AFB1 (0), euthanatized at 25 days; and ethyl maleate and AFB1 (3), 21 days. Clinical signs of toxicosis included decreased feed consumption during AFB1 administration, loss of body weight or failure to gain, and death. Clinicopathologic changes included increases in serum bilirubin concentration and alanine aminotransferase and aspartate aminotransferase activities. Prothrombin and activated partial thromboplastin times were lengthened. Plasma fibrinogen concentration was decreased. Changes in PCV, hemoglobin concentration, and serum alkaline phosphatase were unremarkable. Oxytetracycline had protective effects against chronic aflatoxicosis in rabbits. Cysteine and methionine enhanced chronic aflatoxicosis.     

Effect of methimazole-induced hypothyroidism on adrenal and gonadal functions in male Japanese quail (Coturnix japonica)

To investigate the effect of hypothyroidism on gonadal and adrenal functions in male Japanese quail (Coturnix japonica), hypothyroidism was induced in male adult Japanese quail by daily administration of 2-Mercapto-1-methylimidazole (methimazole) in their drinking water. Four weeks after methimazole treatment, the Japanese quail were sacrificed, and the plasma concentrations of free triiodothyronine (FT3), free thyroxine (FT4), total T3 (TT3), total T4 (TT4), corticosterone, testosterone, LH and immunoreactive (ir) inhibins were measured by radioimmunoassay, the testes and adrenal glands were removed and weighed and the thyroid glands and testes were fixed in 4% paraformaldehyde for histological observation. The results showed that the hypothyroidism induced by methimazole caused a significant decrease in body and testes weight; the plasma levels of FT3, FT4 and TT4 significantly decreased, and the hypothyroid quail possessed a greater number of small follicles and more follicular epithelial cells in the thyroid gland. In addition, hypothyroidism resulted in a significant decrease in the plasma concentrations of corticosterone, LH, testosterone and ir-inhibin. Furthermore, no spermatogenesis was found in the seminiferous tubules of the methimazole treatment groups. These results clearly demonstrate that hypothyroidism caused both gonadal and adrenal disturbances in the adult male Japanese quail.     

Clinical and pathologic changes in acute bovine aflatoxicosis: rumen motility and tissue and fluid concentrations of aflatoxins B1 and M1

Effects of aflatoxin on bovine rumen motility were determined by radiotelemetric techniques. Aflatoxin altered amplitude and/or frequency of rumen contractions in steers given dosages of 0.2, 0.4, 0.6, or 0.8 mg of aflatoxin/kg of body weight. Effects of aflatoxin on rumen motility were dose dependent. An increase in elimination time of aflatoxin from rumen contents was observed in steers given the aflatoxin dosages of 0.4 to 0.8 mg/kg. The increase in elimination time of this toxin facilitates diagnostic capabilities for detecting bovine aflatoxicosis by obtaining rumen contents for analysis for aflatoxin. Aflatoxin M1 was detected in rumen contents from steers at 2 hours after aflatoxin was administered. Thus, intraruminal metabolism of aflatoxin B1 to M1 may occur.     

Effects of aflatoxins in young ponies

Sixteen clinically normal, healthy ponies were randomly assigned to 4 groups and given aflatoxin B1 in doses of 0.045, 0.030, 0.015, and 0 (control) mg/kg of body weight per day for 21 days (or total doses of 0.945, 0.630, 0.315, and 0 mg/kg). The animals were allowed to recover for 3 months and then were reassigned to 4 treatment groups such that each group during the 2nd trial included a pony from each of the groups of the 1st trial. The animals in the new groups were intubated and were given aflatoxin in doses of 0.4, 0.2, 0.1, and 0 (control) mg/kg/day for 5 days ( or total doses of 2.0, 1.0, 0.5, and 0 mg/kg). Venous blood samples were drawn every other day to monitor for toxicosis; examinations were made for RBC and WBC counts, hemoglobin concentration, PCV, serum urea nitrogen, prothrombin time, and serum concentrations of aspartate aminotransferase, iditol dehydrogenase, alkaline phosphatase, albumin, gamma-glutamyl transferase, and arginase. There were no significant differences between treatment groups and controls (given no aflatoxin) in the toxicologic values examined for during the 1st trial. During the 2nd experiment, 2 of the ponies in the large-dose treatment gorup (2.0 mg/kg) demonstrated increased serum enzyme activities. These animals had been in the large-dose (0.945 mg/kg) and median-dose (0.63 mg/kg) groups during the 1st trial. Arginase, iditol dehydrogenase, and gamma-glutamyl transpeptidase activities became increased on the 4th day of treatment and continued to increase until the 6th day of the experiment (1 day after treatment was terminated). These enzymes approached control group values at 10 days after cessation of treatment. These increases were indicative of hepatocellular toxicity. It was concluded that the possibility of equine aflatoxicosis exists although ponies given high quality rations appear to be less susceptible than some other species. Prior exposure to aflatoxins may predispose to clinical toxicity on subsequent exposure, despite lack of expression of clinical signs.     

The Effects of Dietary l-Carnitine Supplementation on Semen Traits,Reproductive Parameters,and Testicular Histology of Japanese Quail Breeders

The present study was conducted to determine the effects of supplemental dietary l-carnitine at different levels on semen traits, reproductive parameters, and testicular histology in male Japanese quail breeders. Forty-five 5-wk-old male Japanese quail breeders were fed the same basal diet that was supplemented with 0 (control), 250, or 500 mg of l-carnitine/kg of diet. There were no significant effects of dietary l-carnitine supplementation at different levels on BW, feed intake, testes weight, fertility rate, hatchability rate of set and fertile eggs, and malonaldehyde production (μg/mL of semen) of male Japanese quail breeders. However, the supplementation of dietary l-carnitine at levels of 250 or 500 mg/kg to a basal diet significantly increased sperm viability and decreased multinucleated giant cells per testes in mature male Japanese quail breeders. Additional studies are required to explore the antioxidant role that l-carnitine has in Japanese quail breeders.