モネンシン

Advice for firefighters: Wear self contained breathing apparatus for fire fighting if necessary. /Monensin sodium salt/

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide. /Monensin sodium salt/

Accidental Release Measures. Personal precautions, protective equipment and emergency procedures: Wear respiratory protection. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal. /Monensin sodium salt/

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.

Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber. Contaminated packaging: Dispose of as unused product. /Monensin sodium salt/

SRP: The scientific literature for the use of contact lenses by industrial workers is inconsistent. The benefits or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

Appropriate engineering controls: Avoid contact with skin, eyes and clothing. Wash hands before breaks and immediately after handling the product. /Monensin sodium salt/

Precautions for safe handling: Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Provide appropriate exhaust ventilation at places where dust is formed. /Monensin sodium salt/

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands. /Monensin sodium salt/

The tolerances for residues of monensin are: (1) Cattle-(i) Liver. 0.10 part per million (ppm). (ii) Muscle, kidney, and fat. 0.05 ppm. (iii) Milk. Not required. (2) Goats-(i) Edible tissues. 0.05 ppm. (3) Chickens, turkeys, and quail. A tolerance for residues of monensin in chickens, turkeys, and quail is not required.

Skin protection: Handle with gloves. /Monensin sodium salt/

Eye/face protection Face shield and safety glasses: Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU). /Monensin sodium salt/

Respiratory protection: For nuisance exposures use type P95 (US) or type P1 (EU EN 143) particle respirator.For higher level protection use type OV/AG/P99 (US) or type ABEK-P2 (EU EN 143) respirator cartridges. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU). /Monensin sodium salt/

Body Protection: Complete suit protecting against chemicals. The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace. /Monensin sodium salt/

An experiment was carried out with male broiler chicks to evaluate the combined effect of monensin (150 mg/kg) & the growth promoters (GPs) Zn bacitracin (BAC, 50 mg/kg), virginiamycin (VIR, 25 mg/kg) & avoparcin (AVO, 20 mg/kg) fed from 7 to 28 days of age on performance, utilization of dietary nutrients, yield of defeathered eviscerated carcases (DEC) & size of various organs. The effect of the GPs in the monensin-unsupplemented diets fed up to 49 d of age on performance & carcase was also determined. Monensin significantly (P < 0.05) depressed food intake, weight gain & food efficiency from 7 to 28 d of age. None of the GPs was able to counteract these effects. However, AVO slightly ameliorated them. AVO also significantly increased food intake & improved gain & food efficiency during 7 to 28, but not 28 to 49 or 7 to 49 d of age. VIR & BAC did not affect performance in either age period. Monensin did not affect the utilisation of dietary dry matter, fat or energy, but it significantly decreased nitrogen utilisation. AVO improved nitrogen & fat utilisation & increased dietary AME(n) content. AME(n) was also increased by VIR. The utilisation of these nutrients was not affected by the interactions between monensin & the GPs. Monensin did not affect yield of the DEC or the relative liver size at 31 d of age. It significantly increased the relative length of the small intestine (SI) & decreased its specific weight. AVO significantly increased yield at 31, but not at 53 d of age. BAC & VIR did not affect this variable. AVO & VIR, but not BAC, at both age periods reduced, at times significantly, the size, length & specific weight of the SI. Our conclusions: BAC, VIR & AVO do not counteract the toxic effect of monensin. The effect of GPs in improving performance decreases & even disappears with age, while their effect in reducing the size of the SI is still evident in 49 day old birds.

In this study, co-admin of the ionophore monensin was not shown to alter blood levels of enrofloxacin or norfloxacin.

The characteristics of the toxic interaction between monensin & tiamulin were investigated in rats. A three-day comparative oral repeated-dose toxicity study was performed in Phase I, when the effects of monensin & tiamulin were studied separately (monensin 10, 30, & 50 mg/kg or tiamulin 40, 120, & 200 mg/kg body weight, respectively). In Phase II, the two compounds were administered simultaneously to study the toxic interaction (monensin 10 mg/kg & tiamulin 40 mg/kg bw, respectively). Monensin proved to be toxic to rats at doses of 30 & 50 mg/kg. Tiamulin was well tolerated up to the dose of 200 mg/kg. After combined administration, signs of toxicity were seen (including lethality in females). Monensin caused a dose-dependent cardiotoxic effect & vacuolar degeneration of the skeletal muscles in the animals given 50 mg/kg. Both compounds exerted a toxic effect on the liver in high doses. After simultaneous administration of the two compounds, there was a mild effect on the liver (females only), hydropic degeneration of the myocardium & vacuolar degeneration of the skeletal muscles. The alteration seen in the skeletal muscles was more marked than that seen after the administration of 50 mg/kg monensin alone.

Cultured rat hepatocytes were treated with potassium cyanide, an inhibitor of cytochrome oxidase; valinomycin, a K+ ionophore; carbonyl cyanide m-chlorophenylhydrazone (CCCP), a protonophore; and the ATP synthetase inhibitor oligomycin. The effect of these agents on the viability of the cells was related to changes in ATP content and the deenergization of the mitochondria. The ATP content was reduced by over 90% by each inhibitor. All of the agents except oligomycin killed the cells within 4 h. With the exception of oligomycin, the mitochondrial membrane potential as measured by the distribution of [3H]triphenylmethylphosphonium collapsed with each of the agents. Monensin, a H+/Na+ ionophore, potentiated the toxicity of cyanide and CCCP, whereas the toxicity of valinomycin was reduced. The effect of cyanide and monesin on the cytoplasmic pH of cultured hepatocytes was measured with the fluorescent probe, 2',7'-biscarboxyethyl-5,6-carboxyfluorescein. Cyanide promptly acidified the cytosol, and the addition of 10 microM monensin caused a rapid alkalinization of the cytosol. A reduction of pH of the culture medium from 7.4 to 6.6 and 6.0 prevented the cell killing both by cyanide alone and by cyanide in the presence of monensin. However, neither monensin nor extracellular acidosis had any effect on the loss of mitochondrial energization in the presence of cyanide. It is concluded that ATP depletion per se is insufficient to explain the cell killing with cyanide, CCCP, and valinomycin. Rather, cell killing is better correlated with a loss of mitochondrial energization. With cyanide an intracellular acidosis interferes with the mechanism that couples collapse of the mitochondrial membrane potential to lethal cell injury.

For more Interactions (Complete) data for MONENSIN (9 total), please visit the HSDB record page.

EC50; Species: Lemna gibba (Inflated Duckweed) age 4 frond; Conditions: freshwater, static renewal, 25 °C; Concentration: 998 ug/L for 7 days (95% confidence interval: 955-1042 ug/L); Effect: decreased population biomass /formulation/

EC50; Species: Lemna gibba (Inflated Duckweed) age 4 frond; Conditions: freshwater, static renewal, 25 °C; Concentration: >1000 ug/L for 7 days; Effect: decreased population carotenoid content /formulation/

EC50; Species: Lemna gibba (Inflated Duckweed) age 4 frond; Conditions: freshwater, static renewal, 25 °C; Concentration: >1000 ug/L for 7 days; Effect: decreased population Chlorophyll A concentration /formulation/

EC50; Species: Lemna gibba (Inflated Duckweed) age 4 frond; Conditions: freshwater, static renewal, 25 °C; Concentration: >1000 ug/L for 7 days; Effect: decreased population Chlorophyll B concentration /formulation/

EC50; Species: Lemna gibba (Inflated Duckweed) age 4 frond; Conditions: freshwater, static renewal, 25 °C; Concentration: 2172 ug/L for 7 days (95% confidence interval: 0-8920 ug/L); Effect: reproduction, decreased progeny counts/numbers /formulation/

TERRESTRIAL FATE: Based on a classification scheme(1), Koc values of 125-5700(2), indicate that monensin is expected to have moderate to no mobility in soil(SRC). The pKa of monensin is estimated as 4.2(3), indicating that this compound will exist almost entirely in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Volatilization of monensin from moist soil surfaces is not expected to be an important fate process given the estimated pKa(3). Monensin is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 5.2X10-23 mm Hg at 25 °C(SRC), determined from a fragment constant method(5). Monensin was degraded 40-75% in soil in 7 day aerobic studies, approximately 20% was attributed to abiotic reactions and the remaining portion was considered biodegradation(6). Other degradation studies indicated half-lives of of 3.8 and 3.3 days in unamended and manure amended soil, respectively(7).

Monensin degraded to trace levels in 20 days in manure amended and unamended field soil plots treated at an initial concentration of 1 ppm; no monensin was detectable after 33 days(1). Monensin was reported as being persistent under anaerobic conditions, with 30-40% biodegradation expected in 10 weeks, but more degradation occurred under aerobic conditions(2). Monensin, applied to agricultural soil May 29, 2004 in Northumberland County, Ontario, Canada at a rate of 1 mg/kg, had degradation half-lives of 3.8 and 3.3 days in unamended soil (organic matter 3.2-3.5%, pH 5.4-5.5) and manure amended soil (organic matter 3.6-4.1%, pH 5.7-5.8), respectively(3).

AQUATIC FATE: Based on a classification scheme(1), Koc values of 125-5700(2), indicate that monensin may be adsorb to suspended solids and sediment(SRC). An estimated pKa of 4.2(3) indicates monensin will exist almost entirely in the anion form at pH values of 5 to 9 and, therefore, volatilization from water surfaces is not expected to be an important fate process(SRC). Monensin was stable to hydrolysis at pH 7 and 9, but had a hydrolysis half-life of 13 days at pH 4 and 25 °C(4). According to a classification scheme(5), an estimated BCF of 10(SRC), from an estimated log Kow of 5.43(6) and a regression-derived equation(6), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data in water were not available, however soil degradation studies, monensin degraded 40-75% in 7 days, approximately 20% was attributed to abiotic reactions and the remaining portion was considered biodegradation(7).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), monensin, which has an estimated vapor pressure of 5.2X10-23 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase monensin may be removed from the air by wet and dry deposition(SRC). Monensin did not absorb light at environmentally relevant wavelengths(3) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

IDENTIFICATION AND USE: Monensin is a polyether carboxylic ionophore antibiotic. Monensin is a mixture of four analogues, A, B, C and D, with monensin A being the major component (98%). Depending on the method of purification, monensin can exist in mycelial, crystalline and recrystallized forms. It is used for the treatment of coccidiosis in poultry (chickens, turkeys and quail) and ruminants (cattle, sheep and goats). Monensin is also used to control ketosis and bloat in cattle and as a growth promoter feed additive in cattle and sheep. Monensin is mainly effective against Gram-positive bacteria. HUMAN EXPOSURE AND TOXICITY: 17 year-old boy who developed myoglobinuria, renal failure and death 11 days after ingesting sodium monensin. In another case, a patient took a dose of monensin three times higher than a dose considered lethal for cattle and developed a clinical picture similar to that reported in veterinary medicine. There was an early and extremely severe rhabdomyolysis followed by acute renal failure, heart failure, and death. The main changes observed at autopsy were extensive skeletal muscle necrosis, complement deposition at the myocardial level, pulmonary edema, & acute tubular damage. ANIMAL STUDIES: Acute toxicity was examined in mature rhesus monkeys. Pairs of monkeys were exposed to a single dose of 20, 40 or 60 mg monensin/kg bw by gavage and were monitored for 7 days. All animals survived and developed diarrhea within 24 hr after dosing. Adult goats were administered sodium monensin, 13.5 mg kg (-1), daily for five consecutive days via gastric gavage. Monensin exposure caused diarrhea, tachycardia and reduction in ruminal movements and body temperature. In an inhalational exposure study, rats were exposed to either normal air or air containing particulate mycelial monensin sodium at a mean concentration of 79 mg/cu m for 2 weeks (1 hr/day, 5 days/week). Nine of 10 treated females became anorexic and lost weight during the 2nd week of the study. Slight focal myositis of the skeletal muscle was seen in two males and two females but none of the controls. Multifocal myocardial changes were observed in male rats treated with monensin. In a subchronic study, male and female mice were fed diets containing 0, 37.5, 75, 150 or 300 mg mycelial monensin sodium/kg for 3 months. A dose-dependent decrease in body weight gain occurred in all dose groups. At the end of the study, the decrease ranged from 27% and 21% in the lowest dose group in females and males, respectively, to 99% in the highest dose group in both sexes. In a chronic toxicity study, male and female rats were maintained on a diet containing 25, 56 or 125 mg crystalline monensin sodium/kg, whereas control rats received a normal diet for 2 years. Body weight and weight gain were significantly decreased in animals receiving 125 mg monensin/kg in their diet and were transiently decreased during the first 4 months in rats in the middle dose group. Benign and malignant neoplasms were observed in treated and untreated animals, with no association between monensin administration and neoplasm type or severity. Monensin is toxic in horses. Clinical signs were tachycardia and cardiac arrythmia, groaning, incoordination, sudoresis, recumbency, and paddling movements with the limbs before death. Main necropsy findings were in the skeletal muscles and myocardium. The effects of exposure to monensin during development were studied in rats. Groups of female rats received monensin at concentrations of 0, 100 or 300 mg/kg until premating weights achieved 185 g and during pregnancy and lactation. Female body weight was significantly decreased in the highest dose group after 8 days of treatment. The body weights of male and female pups in the highest dose group were reduced from postnatal day 10 until postnatal day 21. Male offspring in the low dose group showed body weight reduction only on postnatal day 21. No external signs of malformation were detected in the pups. A study was also undertaken to explore the effects of monensin, a potent Golgi disturbing agent on male fertility. Male rats were administered monensin at the dose levels of 2.5, 5, and 10 mg/kg b wt. Animals were sacrificed after 67 days of the treatment. The findings from electron microscopy such as membrane disruption, swelling and disintegration of Golgi apparatus strongly suggest the interference of monensin with the functioning of Golgi apparatus in the spermatogenic cells. Data from the sperm number and motility as well as the fertility studies and the resulted litter size further points towards the antifertility effects of monensin in male rats. Genotoxicity tests were negative.

/OTHER TERRESTRIAL SPECIES/ A field experiment was initiated whereby a series of replicated plots received annual applications of ivermectin, monensin, and zinc bacitracin, either singly or in a mixture. Pharmaceuticals were added at concentrations of 0.1 mg/kg soil or 10 mg/kg soil. The authors collected soil samples in 2013, before and after the fourth annual application of pharmaceuticals. In addition, a 30-day laboratory experiment was undertaken with the same soil and same pharmaceuticals, but at concentrations of 100 mg/kg soil. The impact of the pharmaceuticals on nitrification rates, on the abundance of ammonia-oxidizing bacteria (AOB), and on the abundance of ammonia-oxidizing archaea (AOA) was assessed. None of the pharmaceuticals at 0.1 mg/kg had any effect on nitrification. Referenced to control soil, nitrification was accelerated in soil exposed to 100 mg/kg zinc bacitracin or 10 mg/kg of the pharmaceutical mixture, but none of the treatments inhibited nitrification. Neither AOB abundance nor AOA abundance was affected by the pharmaceuticals at 0.1 mg/kg. At 10 mg/kg, monensin, zinc bacitracin, and a mixture of all 3 pharmaceuticals suppressed the abundance of AOB, and zinc bacitracin and the mixture increased AOA abundance. The decrease in AOB abundance and increase in AOA abundance when exposed to 10 mg/kg soil suggests that AOB are more sensitive to these chemicals and that AOA populations can expand to occupy the partially vacated niche.

Monensin concentrations in leachate from a livestock mortality pit reached a maximum of 11,980 ng/L at about 200 days post burial, this calculates to an estimated mass loading of 1.01 ug/kg of buried cattle carcass material(1). Monensin was detected in rainfall runoff from poultry litter fertilized soil(2).

Measured Koc values for monensin were 125-5700(1). According to a classification scheme(2), this Koc range suggests that monensin is expected to have moderate to no mobility in soil. The estimated pKa of monensin is 4.2(3), indicating that this compound will exist almost entirely in anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4).

The Koc for monensin was determined in various soils collected from the US and Korea(1).[Table#6643]

/CASE REPORTS/ ... The patient took a dose of monensin three times higher than a dose considered lethal for cattle & developed a clinical picture similar to that reported in veterinary medicine. There was an early & extremely severe rhabdomyolysis followed by acute renal failure, heart failure, & death. The main changes observed at autopsy were extensive skeletal muscle necrosis, complement deposition at the myocardial level, pulmonary edema, & acute tubular damage.

/CASE REPORTS/ ... A case of a 17 year-old boy who developed myoglobinuria, renal failure & death 11 days after ingesting sodium monensin, possibly with the intention of developing muscles /was reported/. /Sodium monensin/

The tolerances for residues of monensin are: (1) Cattle-(i) Liver. 0.10 part per million (ppm). (ii) Muscle, kidney, and fat. 0.05 ppm. (iii) Milk. Not required. (2) Goats-(i) Edible tissues. 0.05 ppm. (3) Chickens, turkeys, and quail. A tolerance for residues of monensin in chickens, turkeys, and quail is not required.

Monensin. New animal drug for use in animal feeds. Conditions of use in broiler chickens, turkeys, cattle, replacement chickens intended for use as cage layers, bobwhite quail, and goats.

The Generic Animal Drug and Patent Restoration act requires that each sponsor of an approved animal drug must submit to the FDA certain information regarding patents held for the animal drug or its method of use. The Act requires that this information, as well as a list of all animal drug products approved for safety and effectiveness, be made available to the public. Monensin is included on this list.

The Generic Animal Drug and Patent Restoration act requires that each sponsor of an approved animal drug must submit to the FDA certain information regarding patents held for the animal drug or its method of use. The Act requires that this information, as well as a list of all animal drug products approved for safety and effectiveness, be made available to the public. Monensin sodium is included on this list. /Monensin sodium/

Factor in antibiotic complex found in Streptomyces cinnamonensis; [Merck Index] Used as veterinary antibacterial and antifungal agent; as feed additive; as growth promoter in ruminants; as medicinal feed additive to treat coccidiosis in chickens and turkeys; [HSDB]

Farming (Feed Additives) [Category: Industry]

MEDICATION (VET)

Antifungal Agents; Antiprotozoal Agents; Coccidiostats

FDA approved medicinal feed additive for chicken and turkey for coccidiosis.

Used commercially as a growth promoter in ruminants.

Synthesized by the preparation and coupling of three fragments and each prepared from commercially available optically active starting materials. /Pharmacueticals, chiral/

Production: Haney, Hoehn, USA patent 3501568 (1970 to Lily).

Monensin is a major component of the antibiotic complex isolated from Streptomyces cinnamonensis.

Oral (Feed): Coban 90 Monesin Granules, Active Drug Ingredient - Monensin, USP - 90.7 g per pound.

Oral (Feed): Rumensin 90 Monensin Granule, Active drug ingredients: Monensin granulated, USP, 90.7 g monensin activity per pound.

Veterinary Drug -> ANTIMICROBIAL_AGENT -> JECFA Functional Classes

Pharmaceuticals -> Animal Drugs -> Approved in Taiwan

Monensin is generally used as the sodium salt. Monensin is a mixture of four analogues, A, B, C and D, which are produced during fermentation, with monensin A being the major component (98%). ... Depending on the method of purification, monensin can exist in mycelial, crystalline and recrystallized forms.

... was found in the mycelium of Streptomyces cinnamonensis by Eil Lilly and Co in 1967 in the course of screening for anticoccidial and growth-promoting substances for cattle, swine, and chickens.