Alum and Rainfall Effects on Ionophores in Runoff from Surface-Applied Broiler Litter.

Polyether ionophores, monensin, and salinomycin are commonly used as antiparasitic drugs in broiler production and may be present in broiler litter (bird excreta plus bedding material). Long-term application of broiler litter to pastures may lead to ionophore contamination of surface waters. Because polyether ionophores break down at low pH, we hypothesized that decreasing litter pH with an acidic material such as aluminum sulfate (alum) would reduce ionophore losses to runoff (i.e., monensin and salinomycin concentrations, loads, or amounts lost). We quantified ionophore loss to runoff in response to (i) addition of alum to broiler litter and (ii) length of time between litter application and the first simulated rainfall event. The factorial experiment consisted of unamended (∼pH 9) vs. alum-amended litters (∼pH 6), each combined with simulated rainfall at 0, 2, or 4 wk after litter application. Runoff from alum-amended broiler litter had 33% lower monensin concentration ( < 0.01), 57% lower monensin load ( < 0.01), 48% lower salinomycin concentration ( < 0.01), and 66% lower salinomycin load ( < 0.01) than runoff from unamended broiler litter when averaged across all events of rainfall. Ionophore losses to runoff were also less when rainfall was delayed for 2 or 4 wk after litter application relative to applying rainfall immediately after litter application. While the weather is difficult to predict, our data suggest that ionophore losses in runoff can be reduced if broiler litter applications are made to maximize dry time after application.

Stacking Time and Aluminum Sulfate Effects on Polyether Ionophores in Broiler Litter.

The use of ionophores as antiparasitic drugs plays an important role in US poultry production, especially in the broiler () industry. However, administered ionophores can pass through the bird's digestive system and appear in broiler litter, which, when applied to agricultural fields, can present an environmental hazard. Stacking (storing or stockpiling) broiler litter for some time might decrease the litter ionophore concentrations before land application. Because ionophores undergo abiotic hydrolysis at low pH, decreasing litter pH with acidic aluminum sulfate (alum) might also decrease ionophore concentrations. We assessed the change in ionophore concentrations in broiler litter in response to the length of time broiler litter was stored (stacking time) and alum addition. We spiked broiler litter with monensin and salinomycin, placed alum-amended litter (∼pH 4-5) and unamended litter (∼pH 8-9) into 1.8-m bins, and repeatedly sampled each bin for 112 d. Our findings showed that stacking broiler litter alone did not have an impact on monensin concentration, but it did slowly reduce salinomycin concentration by 55%. Adding alum to broiler litter reduced monensin concentration by approximately 20% relative to unamended litter, but it did not change salinomycin concentration. These results call for continued search for alternative strategies that could potentially reduce the concentration of ionophores in broiler litter before their application to agricultural soils.

Genetic analysis of tissue glutathione concentrations and redox balance.

Glutathione redox balance-defined as the ratio GSH/GSSG-is a critical regulator of cellular redox state, and declines in this ratio are closely associated with oxidative stress and disease. However, little is known about the impact of genetic variation on this trait. Previous mouse studies suggest that tissue GSH/GSSG is regulated by genetic background and is therefore heritable. In this study, we measured glutathione concentrations and GSH/GSSG in liver and kidney of 30 genetically diverse inbred mouse strains. Genetic background caused an approximately threefold difference in hepatic and renal GSH/GSSG between the most disparate strains. Haplotype association mapping determined the loci associated with hepatic and renal glutathione phenotypes. We narrowed the number of significant loci by focusing on those located within protein-coding genes, which we now consider to be candidate genes for glutathione homeostasis. No candidate genes were associated with both hepatic and renal GSH/GSSG, suggesting that genetic regulation of GSH/GSSG occurs predominantly in a tissue-specific manner. This is the first quantitative trait locus study to examine the genetic regulation of glutathione concentrations and redox balance in mammals. We identified novel candidate genes that have the potential to redefine our knowledge of redox biochemistry and its regulation and inform future therapeutic applications.