PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Roxarsone”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

Environmental fate of roxarsone in poultry litter. I. Degradation of roxarsone during composting.

Roxarsone, 3-nitro-4-hydroxyphenylarsonic acid, is an organoarsenic compound that is used extensively in the feed of broiler poultry to control coccidial intestinal parasites, improve feed efficiency, and promote rapid growth. Nearly all the roxarsone in the feed is excreted unchanged in the manure. Poultry litter composed of the manure and bedding material has a high nutrient content and is used routinely as a fertilizer on cropland and pasture. Investigations were conducted to determine the fate of poultry-litter roxarsone in the environment Experiments indicated that roxarsone was stable in fresh dried litter; the primary arsenic species extracted with water from dried litter was roxarsone. However, when water was added to litter at about 50 wt % and the mixture was allowed to compost at 40 degrees C, the speciation of arsenic shifted from roxarsone to primarily arsenate in about 30 days. Increasing the amount of water increased the rate of degradation. Experiments also suggested that the degradation process most likely was biotic in nature. The rate of degradation was directly proportional to the incubation temperature; heat sterilization eliminated the degradation. Biotic degradation also was supported by results from enterobacteriaceae growth media that were inoculated with litter slurry to enhance the biotic processes and to reduce the concomitant abiotic effects from the complex litter solution. Samples collected from a variety of litter windrows in Arkansas, Oklahoma, and Maryland also showed that roxarsone originally present had been converted to arsenate.

Animal Feed↗

NTP Toxicology and Carcinogenesis Studies of Roxarsone (CAS No. 121-19-7) in F344/N Rats and B6C3F1 Mice (Feed Studies).

Roxarsone is a veterinary drug used as a growth promoter and as an anticoccidial agent and for treatment of swine dysentery. Toxicology and carcinogenesis studies were conducted by administering roxarsone (greater than 99.4% pure) in feed to groups of F344/N rats and B6C3F1 mice of each sex for 14 days, 13 weeks, or 2 years. Fourteen-Day and Thirteen-Week Studies: In the 14-day studies, the diets fed to rats contained 0 or 100-1,600 ppm roxarsone, and those fed to mice contained 0 or 60-1,000 ppm. Deaths occurred in rats and mice that received the highest doses. Rats that received 800 or 1,600 ppm lost weight. Male mice that received 1,000 ppm and female mice that received 500 ppm lost weight. In the first 13-week studies, roxarsone was fed to rats and mice at dietary concentrations of 0 or 50-800 ppm. Decreases (more than 10%) in final mean body weights of dosed rats relative to those of controls were observed for males that received 200, 400, or 800 ppm and for females that received 400 or 800 ppm. Deaths occurred in groups that received 800 ppm. Clinical signs of toxicity (trembling, ataxia, and pale skin) were seen primarily in rats that received 800 ppm. Kidney lesions were observed in rats that received 800 ppm. These lesions were characterized by tubular necrosis and mineralization in the rats that died during the studies and by tubular dilatation and casts, interstitial inflammation, and tubular epithelial cell regeneration in the rats that lived to the end of the studies. Additional 13-week studies were conducted in rats at dietary concentrations of 0, 100, or 400 ppm to demonstrate the absorption of roxarsone from the gastrointestinal tract; to determine its distribution in liver, kidney, and blood; and to study its effects on various hematologic and clinical chemical values. No deaths occurred. Renal lesions of minimal severity observed in male rats that received 400 ppm were characterized by tubular epithelial cell degeneration and regeneration, tubular casts, and mineralization. Arsenic levels in urine, blood, kidney, and liver of dosed rats increased (140%-300%) with time on study and were proportional to the dietary concentrations of roxarsone. No compound-related hematologic or clinical chemical effects were observed in rats. In the first 13-week studies, final mean body weights of mice that received 800 ppm were 11%-18% lower than those of controls. Deaths occurred in males and females receiving 400 and 800 ppm. No compound-related gross or histopathologic lesions were observed. In the second 13-week studies in mice, no compound-related hematologic or clinical chemical effects were observed. At the end of the studies, arsenic concentrations in dosed mice ranged from 0.45 to 0.99 ug/g of liver and from 0.85 to 2.98 ug/g of kidney. No arsenic was detected in the liver or kidney of control mice. Because of kidney lesions, lower body weight gain, and increased mortality in rats and lower body weight gain and increased mortality in mice in the short-term studies, dietary concentrations of roxarsone selected for the 2-year studies were 0, 50, or 100 ppm for rats and 0, 100, or 200 ppm for mice. Body Weight and Survival in the Two-Year Studies: Mean body weights of dosed rats were generally within 5% of those of controls. No significant differences in survival were observed between any groups of rats of either sex, although survival in males was lower than usual (final survival--male: control, 24/50; low dose, 18/50; high dose, 18/50; female: 27/50; 35/50; 32/50). The average feed consumption by high dose rats was 95% that of controls for males and 88% for females. The average amount of roxarsone consumed per day was approximately 2 mg/kg for low dose rats and 4 mg/kg for high dose rats. Mean body weights of high dose male mice were generally 5%-8% higher than those of the controls, whereas those of female mice were generally 6%-15% lower than those of the controls. The survival of the control group of male mice was lower than that of the low dose group after month 22; survival for females was low (final survir than that of the low dose group after month 22; survival for females was low (final survival--male: 27/50; 40/50; 33/50; female: 14/50; 18/50; 17/50). The low survival in females was due in part to utero-ovarian infection, with more than 50% of the animals in each dose group having suppurative inflammation at this site. The average daily feed consumption by dosed mice was 105%-110% that by the controls. The average amount of roxarsone consumed per day was approximately 21 or 43 mg/kg for low dose or high dose male mice and 27 or 54 mg/kg for low dose or high dose female mice. Nonneoplastic and Neoplastic Effects in the Two-Year Studies: Although the incidence of adenomas of the exocrine pancreas in high dose male rats was not statistically greater than that in the controls (control, 1/50; low dose, 1/50; high dose, 5/50), it was greater than that seen in any historical control group of male F344/N rats. The historical rate is 1/437 (0.2%) for the study laboratory and 5/1,871 (0.3%) throughout the Program. The incidences of hyperplasia were 2/50; 0/50; 3/50. No hyperplasia oradenomas were observed in the exocrine pancreas of female rats. Clitoral gland adenomas in female rats occurred with a marginally positive trend (1/44; 3/47; 6/48; P=0.049). One carcinoma was also observed in each of the groups. The incidences of adenomas or of adenomas or carcinomas (combined) in the dosed groups were not significantly different from those in the controls. This marginal effect was not considered to be related to roxarsone administration. No chemical-related increases in neoplastic or nonneoplastic lesions occurred in male or female mice. Lymphomas in female mice occurred with a negative trend; the incidences in the dosed groups were lower than that in the controls (13/50; 2/50; 3/50; P≤0.01). Genetic Toxicology: Roxarsone was not mutagenic in Salmonella typhimurium strains TA98, TA100, TA1535, or TA1537 with or without metabolic activation. Roxarsone induced trifluorothymidine (Tft) resistance in mouse lymphoma L5178Y cells in the absence of metabolic activation; it was not tested with activation. Exposure of adult male Drosophila melanogaster to roxarsone by injection or by feeding did not cause an increase in sex--linked recessive lethal mutations. Audit: The data, documents, and pathology materials from the 2-year studies of roxarsone have been audited. The audit findings show that the conduct of the studies is documented adequately and support the data and results given in this Technical Report. Conclusions: Under the conditions of these 2-year feed studies, there was equivocal evidence of carcinogenic activity of roxarsone for male F344/N rats, as indicated by a marginally increased incidence of adenomas of the exocrine pancreas. There was no evidence of carcinogenic activity for female F344/N rats fed diets containing 50 or 100 ppm roxarsone for 2 years. There was no evidence of carcinogenic activity for male or female B6C3F1 mice fed diets containing 100 or 200 ppm roxarsone for 2 years. Synonyms: 4-hydroxy-3-nitrophenylarsonic acid; 4-hydroxy-3-nitrobenzenearsonic acid; 2-nitro-1-hydroxybenzene-4-arsonic acid; nitrophenolarsonic acid; 3-nitro-4-hydroxybenzenearsonic acid; 3-nitro-4-hydroxyphenylarsonic acid Trade Names: Ristat; Ren-O-sal; 3-nitro; 3-nitro-10; 3-nitro-20; 3-nitro-50; 3-nitro-80

Journal Article↗

Interactive effects of monensin, roxarsone, and copper in young chickens infected with Eimeria tenella or a combination of E: tenella and E. acervulina.

Experiments were conducted with crossbred male chicks to evaluate the interactions among roxarsone (50 mg/kg), monensin (121 mg/kg), and copper sulfate (100 mg/kg) as treatments for experimental Eimeria tenella and E. acervulina infections. When diets containing monensin, roxarsone, or a combination of both were offered to chicks for 15 min or 1, 3, 5, or 8 days prior to E. tenella challenge (5 X 10(4) sporulated oocysts), monensin fed for 15 min or roxarsone fed for 1 day prior to challenge prevented morbidity. A mixed infection of E. tenella and E. acervulina (5 X 10(4) and 4 X 10(5) sporulated oocysts, respectively) reduced gain and gain:feed conversion ratios and caused severe duodenal and cecal lesions at Day 6 of the experiment. Infected chicks gained faster when diets were supplemented with either monensin or roxarsone, but monensin produced a larger response than roxarsone. The mixed infection decreased shank pigmentation, with amelioration activity evident from monensin but not from roxarsone. Lesion scores at Day 6 indicated markedly reduced lesions in the duodenum due to monensin but not due to roxarsone; likewise, reductions in cecal lesions occurred in birds fed roxarsone but less so in birds fed monensin. Lesion scores showed little evidence of additivity due to monensin and roxarsone. In general, copper sulfate exerted no independent or interactive effect on any of the parameters evaluated. In a subsequent experiment, the effect of feeding roxarsone in combination with the biological reducing agent, cysteine, was evaluated in E. tenella-infected chicks. Rate and efficiency of gain were improved and lesion scores were reduced by supplementary roxarsone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Toxic effects of supplemental copper and roxarsone when fed alone or in combination to young pigs.

Three experiments were conducted to investigate the roxarsone (3-nitro-4-hydroxyphenylarsonic acid) X copper (Cu) interaction in weanling pigs. Supplemental roxarsone at 400 mg/kg diet decreased rate and efficiency of weight gain and caused visible neurological signs of toxicosis. Copper addition (CuSO4 X 5H2O) at a level of 650 mg Cu/kg diet likewise decreased weight gain and feed efficiency, and it also increased hepatic Cu deposition. The combination of these growth-depressing dosages of roxarsone and Cu resulted in a far greater reduction in gain and efficiency of feed utilization than was the case when either compound was fed alone. A growth-promoting dosage of Cu (250 mg/kg) increased weight gain by 32% in one experiment but showed no efficacy in alleviating the growth-depression resulting from feeding 400 mg/kg roxarsone. A roxarsone dosage of 100 mg/kg increased gain and feed efficiency. Surprisingly, the decreased weight gain in pigs fed 650 mg/kg Cu was ameliorated by feeding 100 mg/kg roxarsone concomitantly. This level of roxarsone also reduced liver Cu concentration substantially. It thus appears that the nature of the roxarsone X Cu interaction is dependent on the dose of each compound administered. Moreover, low-dose roxarsone administration appears to ameliorate Cu toxicity, but low-dose Cu feeding does not show efficacy against roxarsone toxicity.

Animals↗

Effects of roxarsone on pigmentation and coccidiosis in broilers.

Roxarsone (0.005%) medicated chickens inoculated at seven weeks of age with Eimeria maxima oocysts had significantly higher pigment levels in blood plasma than did unmedicated controls. Unmedicated E. maxima infected birds had significantly lower pigment levels compared to uninoculated controls. Uninoculated roxarsone medicated controls showed no increase in pigment levels over uninoculated unmedicated birds. This experimental design demonstrates that the beneficial effect of roxarsone medication is due to anticoccidial action rather than an increase in pigmentation after feeding the yellow-colored roxarsone. Since uninoculated birds gained more rapidly if roxarsone (0.025%) was added to the diet, the drug also appears to stimulate growth as well as to protect against coccidial infection. In two floor-pen experiments roxarsone demonstrated anticoccidial activity as measured by higher pigment scores than unmedicated infected controls. The coccidial infection was induced after seeding the litter with oocysts from birds infected with E. acervulina, E. brunetti, E. hagani, E. maxima, E. mivati, E. necatrix, E. praecox, and E. tenella. Pigmentation levels were significantly higher in plasma and skin of roxarsone medicated chickens in two experiments and in shanks in one experiment. Similar protection against depigmentation was demonstrated by adding roxarsone to feed medicated with nequinate. These results involving addition of roxarsone may explain some equivocal reports on pigmentation, weight gains or feed conversion. Some previous investigators appear to have used an inadequate experimental design by omitting use of unmedicated uninoculated controls or to have made no attempt to monitor for presence or absence of coccidiosis.

Animals↗

Effects of roxarsone and monensin on digital flexoral tendons of broiler chickens.

Roxarsone and monensin are common poultry feed additives that are used alone or in combination with other drugs to improve growth and feed utilization in young birds. The effects of monensin and roxarsone on the physiology of flexoral tendons of broiler chickens were examined to understand their relationships to leg weakness that have been occasionally associated with these drugs. Day-old chickens were fed either roxarsone or monensin for a period of 6 wk with two regimens of each of the drugs (roxarsone, 45.4 or 90.8 g/ton feed; monensin, 100 or 150 g/ton feed). None of the treatments had any adverse effect on the growth of the birds or caused any significant leg problem. Roxarsone at 45.4 g/ton caused a significant gain in body weight. The biomechanical strength of digital flexoral tendons was measured in several ways. There were no statistical differences in load at break, the modulus of elasticity, or stress or strain levels between different treatment groups and birds that received no medication. There were no differences in collagen, proteoglycan, and pyridinoline content of tendons. Sequential extraction of tendons with different solvents revealed a significant increase in the percentage of guanidine HCl extractible collagens in monensin-treated birds, and a decrease in the acid extractible collagen in both roxarsone- and monensin-treated groups. The relative content of collagen in acid extractible collagens were significantly small relative to total collagen content. Majority of collagen (84 to 90%) was extractible with pepsin. About 8 to 11% of total collagen was resistant to pepsin that was extractible with collagenase; this did not differ between treatment groups. Roxarsone treatment had no effect on the guanidine soluble collagen pool. The effect of monensin on the increase in guanidine soluble pool of collagen may relate to its disruptive effects on cellular secretory processes, which may be of significance in modulating connective tissue function in conjunction with other factors. However, in the present study, neither roxarsone nor monensin alone produced any significant leg problems nor caused any significant differences in the physiology of flexoral tendons or altered their biomechanical properties.

Amino Acids↗

Long-term broiler performance with bambermycins and bambermycins plus roxarsone.

Bambermycins and bambermycins plus roxarsone were fed to broilers in ten consecutive experiments to determine if response (measured by body weight and feed efficiency) was continuous over a long term. Bambermycins was added at 1.1 ppm (1 to 44 days) and 2.2 ppm (45 to 51 days) to both test rations. In addition, one test ration contained roxarsone (3-nitro-4-hydroxyphenylarsonic acid) at 50 ppm (1 to 44 days). Each experiment was conducted with 1,080 commercial broiler cross-run chickens. Broilers fed bambermycins and bambermycins plus roxarsone were heavier (P less than .05) than controls in every experiment. Bambermycins plus roxarsone treated broilers were heavier (P less than .05) than bambermycins treated broilers in 2 out of 10 experiments. Broilers fed bambermycins converted feed more efficiently (P less than .05) than controls in 6 of 10 experiments and were more efficient (P less than .05) than bambermycins plus roxarsone fed broilers in 1 of 10 experiments. Bambermycins plus roxarsone treated broilers were more efficient (P less than .05) than controls in 5 of 10 experiments. These findings indicate that over a long term bambermycins and bambermycins plus roxarsone consistently and significantly (P less than .05) increased broiler body weights over controls, although the addition of roxarsone was not always effective in increasing body weights or improving feed efficiency over bambermycins fed alone.

Animals↗

Photodegradation of roxarsone in poultry litter leachates.

Arsenic compounds have been used extensively in agriculture in the US for applications ranging from cotton herbicides to animal feed supplements. Roxarsone (3-nitro-4-hydroxyphenylarsonic acid), in particular, is used widely in poultry production to control coccidial intestinal parasites. It is excreted unchanged in the manure and introduced into the environment when litter is applied to farmland as fertilizer. Although the toxicity of roxarsone is less than that of inorganic arsenic, roxarsone can degrade, biotically and abiotically, to produce more toxic inorganic forms of arsenic, such as arsenite and arsenate. Experiments were conducted on aqueous litter leachates to test the stability of roxarsone under different conditions. Laboratory experiments have shown that arsenite can be cleaved photolytically from the roxarsone moiety at pH 4-8 and that the degradation rate increases with increasing pH. Furthermore, the rate of photodegradation increases with nitrate and natural organic matter concentration, reactants that are commonly found in poultry-litter-water leachates. Additional photochemical reactions rapidly oxidize the cleaved arsenite to arsenate. The formation of arsenate is not entirely undesirable, because it is less mobile in soil systems and less toxic than arsenite. A possible mechanism for the degradation of roxarsone in poultry litter leachates is proposed. The results suggest that poultry litter storage and field application practices could affect the degradation of roxarsone and subsequent mobilization of inorganic arsenic species.

Animals↗

Roxarsone toxicity in the chick as influenced by dietary cysteine and copper and by experimental infection with Eimeria acervulina.

A series of experiments was conducted with crossbred chicks to determine the effects of L-cysteine, copper, and coccidiosis on roxarsone toxicity. Levels of roxarsone in excess of 50 mg/kg depressed performance and increased kidney arsenic concentration. L-cysteine x HCl x H2O (59%) increased rate and efficiency of gain when added to the basal diet, but depressed performance, increased kidney arsenic concentration, and enhanced mortality when added to diets containing toxic levels of roxarsone (200 mg/kg or higher). Moreover, excess copper (500 mg/kg) partially alleviated the gain/feed depression due to the combination of cysteine and roxarsone. Cysteine, in fact, increased feed efficiency in birds fed excess copper in the absence of roxarsone. Eimeria acervulina infection (duodenal coccidiosis) depressed gain and feed efficiency. The depression in feed efficiency was more severe in the presence of roxarsone (50 or 300 mg/kg). In the absence of coccidiosis, 50 mg/kg roxarsone slightly increased gain/feed ratio.

Animals↗

Response of broiler chickens to dietary supplementation with roxarsone and bacitracin methylene disalicylate in diets containing narasin.

Six trials were conducted at different locations to examine the response of broiler chickens to roxarsone and bacitracin in the form of bacitracin methylene disalicylate (BMD) in the presence of the anticoccidal narasin. All diets contained narasin (80 mg/kg) and were fortified with a factorial arrangement of roxarsone (0 to 50 mg/kg) and BMD (0 or 55 mg/kg). Broilers were grown to market weights with narasin and roxarsone removed from the diets for the final 5 days. Addition of both roxarsone and BMD resulted in significant (P less than .05) improvements in body weight and feed utilization. Response to roxarsone for feed utilization was influenced to some extent by the presence or absence of BMD. Although the response to roxarsone was always positive, the degree of response was lessened by the presence of BMD. This resulted in a significant (P less than .10) interaction between roxarsone and BMD for feed utilization but not for body weight.

Animal Feed↗

Sensitive method for the determination of roxarsone using solid-phase microextraction with multi-detector gas chromatography.

We describe the development, optimization, and application of a novel method for the unequivocal identification and quantification of roxarsone (3-nitro-4-hydroxyphenylarsonic acid, 3-NHPAA) at low microg L(-1) levels. The method is based on capillary gas-liquid chromatography with parallel quadrupole ion-trap mass spectrometric (QIT-MS) and pulsed flame photometric detection (PFPD). The sensitive method couples the arsenic specificity of PFPD with the high selectivity of molecular MS for the determination of roxarsone, dimethylarsenic acid (DMAA), and monomethylarsonic acid (MMAA) in complex matrices. Analytes were derivatized based on the approach we previously reported [B. Szostek, J.H. Aldstadt, J. Chromatogr. A 807 (1998) 253 and D.R. Killelea, J.H. Aldstadt, J. Chromatogr. A 918 (2001) 169] for the reaction of organoarsenicals with 1,3-propanedithiol (PDT). The cyclic dithiaarsenolines formed were extracted from the sample matrix in the liquid phase by solid-phase microextraction (SPME). The optimized SPME conditions employed a 65 microm polydimethlysiloxane-divinylbenzene (PDMS-DVB) fiber, extraction temperature of 70 degrees C and fiber equilibration time of 15.0 min. The mass spectrum of the dithiaarsenoline of roxarsone showed a base peak that corresponded to the predicted structure at m/z 319 and the tell-tale peak of an arsenic compound derivatized with PDT at m/z 181. Further peaks at m/z 149 and 228 were observed and found to be unique to roxarsone, formed by an interesting internal rearrangement of the ONOH functionality. A linear calibration model was prepared for roxarsone over an environmentally relevant range (0.0-100 microg L(-1)) and a detection limit of 2.69 microg L(-1) (3sigma) was observed. The method was applied to several fortified environmental surface water samples (50 microg L(-1)) where the average recovery for roxarsone was 103+/-10.9%.

Calibration↗

Effects of lasalocid and monensin in combination with roxarsone on lesion reduction and oocyst suppression in chicks infected with Eimeria tenella field isolates.

The anticoccidial activity of lasalocid, monensin, and roxarsone, alone and in combination, was evaluated against eleven Eimeria tenella recent field isolates. Lasalocid was used at 0.0075. 0.01, and 0.0125% activity drug in feed; monensin at 0.0099 and 0.0121%; and roxarsone at 0.005%. Further studies with lasalocid 0.0075%, monensin 0.0099% and roxarsone 0.005 and 0.0025% combinations were carried out against three E. tenella field isolates selected from the aforementioned strains. Lasalocid and monensin each exhibited a high degree of anticoccidial activity at all concentrations tested. Lasalocid and monensin fed in combination with roxarsone showed, in addition to high anticoccidial activity a further reduction in gross lesions and oocysts production, more pronounced at 0.005% level of roxarsone than at 0.0025%, compared to either medication alone or the roxarsone combinations. These positive effects were noted with all strains tested. The practical aspects of these findings are discussed.

Administration, Oral↗

The effect of zinc bacitracin and roxarsone on performance of broiler chickens when fed in combination with narasin.

Six trials were conducted at various locations to determine the response of broiler chickens to combinations of zinc bacitracin and roxarsone when fed in the presence of narasin. The addition of zinc bacitracin at 55 mg per kg significantly improved growth rate and feed utilization when data from all locations were combined. There was no effect of roxarsone fed at 50 mg per kg on BW or feed utilization, nor was there an interaction of roxarsone and zinc bacitracin on BW. There was a significant interaction of roxarsone and zinc bacitracin for feed utilization; addition of zinc bacitracin significantly improved feed utilization both in the presence and absence of roxarsone, but the improvement was greater in the absence of roxarsone.

Animal Feed↗

Toxic responses in F344 rats and B6C3F1 mice given roxarsone in their diets for up to 13 weeks.

Thirteen-week toxicity studies were conducted in groups of 10 F344 rats and B6C3F1 mice of each sex fed roxarsone at 0, 50, 100, 200, 400, or 800 ppm in the diet. Arsenic levels in blood, urine, kidneys, and liver of rats were measured in additional animals of each sex dosed with 100 or 400 ppm roxarsone. Compound-related mortality occurred in both sexes of rats at 800 ppm and mice at 800 and 400 ppm. Significant body weight gain depression occurred in both sexes of rats at 200, 400, and 800 ppm and mice at 800 ppm. Clinical signs of toxicity (trembling, ataxia, and pale skin) were seen primarily in rats and mice at 800 ppm. Lesions associated with roxarsone administration were noted only in the kidney of rats and were characterized by tubular necrosis and mineralization at the corticomedullary junction. Arsenic levels in urine, blood, liver, and kidneys increased over time and were directly proportional to the level of roxarsone in feed. These levels were greater than 6 times higher in rats than in mice and were about 2 time higher in males than in females. The no-observable-effect level for roxarsone toxicity was estimated at 100 ppm for rats and 200 ppm for mice. No hematology or clinical chemistry effects were found in rats or mice of either sex.

Animals↗

Effect of roxarsone inclusion in the diet on the performance and hepatic lipid metabolism of laying Tsaiya duck.

1. The aim of this study was to examine the effects of roxarsone (3-nitro-4-hydroxyphenylarsonic acid) inclusion in the diet on the performance, liver function and lipid metabolism in the liver of laying Brown Tsaiya ducks. 2. Sixty 36-week-old laying ducks were selected and allocated at random into 4 dietary treatments with 3 replications for each treatment. Feeding was for 7 weeks with 3 weeks of experimental diets followed by a 4 week withdrawal period. The experimental diets were supplemented with 0, 50, 100 and 300 mg/kg roxarsone, respectively 3. Dietary inclusion of 50 or 100 mg/kg roxarsone did not significantly promote performance. Inclusion of 300 mg/kg significantly depressed (P<0.05) performance, liver weight and content, serum triacylglycerol (TG), serum nonesterified fatty acid (NEFA) and increased (P<0.05) cholesterol, creatine kinase (CK) and aspartate aminotransferase (AST) in the serum at the end of 3 weeks on the experimental diet. 4. Laying characteristics returned to normal 4 weeks after withdrawal of roxarsone. The liver weight, fat and TG in the liver and serum concentrations of TG, NEFA, high density lipoprotein (HDL) and AST increased significantly (P<0.05), while the level of very low density lipoprotein (VLDL) decreased (P<0.05) at the end of the withdrawal period. More prominent vacuolised hepatic fatty cells were observed in laying ducks treated with 300 mg/kg of roxarsone.

Animals↗

Feed additive interactions in the chicken: reduction of tissue copper deposition by dietary roxarsone in healthy and in Eimeria acervulina-infected or Eimeria tenella-infected chicks.

Interactions among roxarsone, copper, and coccidiosis were studied in growing crossbred chicks. Corn-soy or corn-soy-corn gluten meal diets were fed in all assays. In the absence of supplemental copper, 50 mg/kg roxarsone did not affect gain. However, in the presence of 250 mg/kg supplemental copper, there was a depression in gain due to feeding 50 mg/kg roxarsone. In contrast, at a toxic level of copper (1000 mg/kg), a growth response resulted from feeding roxarsone. In all instances, roxarsone markedly decreased liver copper concentration in birds fed high levels of copper. Multiple crop intubations of Eimeria acervulina or Eimeria tenella depressed performance and exacerbated copper toxicity symptoms. Copper supplementation as well as coccidial infection resulted in depressed plasma pigmentation.

Animals↗

Response of broiler chickens to addition of bacitracin methylene disalicylate and roxarsone to diets containing halofuginone.

Studies were conducted at six locations over a 7-yr period to evaluate the response of broiler chickens to bacitracin methylene disalicylate (BMD) and roxarsone in the presence of diets containing 3 ppm halofuginone/kg feed. Treatments consisted of a 2 x 2 factorial arrangement with 0 or 55 mg BMD and 0 or 50 mg roxarsone/kg feed. These additives were fed beginning with day-old chicks and were removed 6 days before termination of the study, which varied in length from 48 to 56 days among locations. Body weights were significantly improved (P less than .05) by the addition of either BMD or roxarsone with a significant interaction (P less than .05) between BMD and roxarsone. Roxarsone improved body weights only in the presence of BMD. Feed utilization was significantly (P less than .05) improved by addition of either BMD or roxarsone, with no interaction between the two products.

Animal Feed↗

Effect of narasin and roxarsone combinations on Eimeria tenella infections in floor pen-raised broilers.

A series of four floor pen trials was conducted to evaluate the effects of narasin and roxarsone, both alone and in combination, on their capacity to control severe Eimeria tenella infections in broilers. Three levels of narasin (0, 60, and 80 ppm) were fed to chickens receiving either 0, 25, or 50 ppm roxarsone in a factorial design. Cecal coccidiosis was induced by seeding the litter with ionophore-tolerant and ionophore-sensitive strains of E. tenella. After 8 days, 10 birds/pen were killed and their cecal lesions scored. Performance (body weight and feed consumption) and mortality were measured at the termination of the trials. Narasin reduced the severity of cecal coccidiosis as measured by a reduction in cecal lesions and an improvement in bird performance. Roxarsone also reduced cecal lesion scores. The highest level of roxarsone (50 ppm) in combination with 60 or 80 ppm narasin produced additive responses in the control of E. tenella infections. Maximum performance was obtained when narasin alone was fed at 80 ppm; drug combinations improved performance when compared with that of nontreated or roxarsone only-medicated groups.

Animals↗