Intrinsic in the equation for successful animal production is the efficiency of nutrient use for assimilation into useful animal-derived products. However, when young growing animals encounter various stressors that activate the proinflammatory response (PR), the biochemical effects of the resulting cascade of PR mediators [cytokines, prostaglandin and prosta-cyclin derivatives, nitric oxide (NO), superoxide anion (O2(.-)), etc.] override the regulatory signals normally ascribed to anabolic tissue accretion and growth. The efficiency of energy and nutrient use will proportionally decrease for growth rate due to the redirection of nutrient use to support immune defense processes. These proinflammatory events can develop in association with infectious disease but also are apparent in and a part of the natural response to birth, parturition, and weaning. If growth patterns are tracked during the PR, growth deficits are often apparent. Some growth deficits are relatively transient in duration, whereas others are quite long lasting, persisting although traditional clinical markers of PR are no longer evident. Recent evidence indicates that the PR cascades initiated by cytokines like tumor necrosis factor-alpha play a major role in these growth deficits. Perturbations in mitochondrial energetics and NO and O2(.-) interactions further affect metabolic balance. Free radicals and reactive nitrogen intermediates interact with select molecular targets in proteins (i.e., enzymes, histone proteins, and signal transduction proteins), causing the nitration and nitrosylation of select amino acids. If these posttranslational modifications occur in proteins associated with control points critical in metabolic stability, the resulting altered protein structure blocks its functionality. Attenuation of these overt posttranslational protein modifications at their site of production offers a strategy to minimize their detrimental impact while preserving needed cytokine, NO, and O2(.-) functions.
The ionophoretic antibiotics, monensin and lasalocid, bind numerous mono- and divalent cations, primarily in dimeric complexes that facilitate the passage of metal ions through hydrophobic lipid membranes. Ionophores vary in their affinity for metal ions. Similarly, transport rates of the resulting complexes depend in part upon the affinity constant of the drug ion-binding interaction, and in part, upon local environmental and physical factors. The normal uptake, transport and use of divalent minerals in the animal body is accomplished via numerous endogenous "ionophore" transport routes. We studied the possibility that exogenous ionophores such as monensin and lasalocid might alter normal intestinal uptake of divalent metal ions. In the first experiment, chickens were fed either monensin or lasalocid; 45Ca, 59Fe or 64Cu was individually instilled into an exteriorized isolated loop of the duodenum and absorption allowed for 1 h. Radioactivity was measured in the duodenal mucosa. Compared with controls, 59Fe and 64Cu were lower in tissues from animals given monensin, but higher in animals given lasalocid. 45Ca was lowered in gut mucosa by both drugs. In the second experiment, liver Cu, Fe and Zn were measured in chickens and sheep fed diets containing monensin or lasalocid. Small differences in basal tissue levels of ions were observed in both sheep and chickens fed the ionophoretic drugs. Drenching sheep with 100 mg X animal-1 X d-1 Cu2+ as CuSO4 resulted in enhanced Cu accumulation in all animals, with the largest accumulation measured in those fed monensin. These preliminary data suggest that adding monensin and lasalocid to diets may change the bioavailability, gut uptake and tissue deposition of divalent minerals.(ABSTRACT TRUNCATED AT 250 WORDS)
Accumulation of heavy metals such as zinc (Zn) disturbs the metabolism of reactive oxygen (e.g. hydrogen peroxide, H2O2) and nitrogen species (e.g. nitric oxide, NO; S-nitrosoglutathione, GSNO) in plant cells; however, their signal interactions are not well understood. Therefore, this study examines the interplay between H2O2 metabolism and GSNO signaling in Arabidopsis. Comparing the Zn tolerance of the wild type (WT), GSNO reductase (GSNOR) overexpressor 35S::FLAG-GSNOR1 and GSNOR-deficient gsnor1-3, we observed relative Zn tolerance of gsnor1-3, which was not accompanied by altered Zn accumulation capacity. Moreover, in gsnor1-3 plants Zn did not induce NO/S-nitrosothiol (SNO) signaling, possibly due to the enhanced activity of NADPH-dependent thioredoxin reductase. In WT and 35S::FLAG-GSNOR1, GSNOR was inactivated by Zn, and Zn-induced H2O2 is directly involved in the GSNOR activity loss. In WT seedlings, Zn resulted in a slight intensification of protein nitration detected by Western blot and protein S-nitrosation observed by resin-assisted capture of SNO proteins (RSNO-RAC). LC-MS/MS analyses indicate that Zn induces the S-nitrosation of ascorbate peroxidase 1. Our data collectively show that Zn-induced H2O2 may influence its own level, which involves GSNOR inactivation-triggered SNO signaling. These data provide new evidence for the interplay between H2O2 and SNO signaling in Arabidopsis plants affected by metal stress.
Twenty multiparous ewes and their newborn lambs were assigned to a 2 x 2 factorial experiment in which ewes were fed ad libitum either a moderate (MP, 15%) or a low (LP, 10%) CP diet and nursed either twin (T) or single (S) lambs. Nitrogen (N) balance trials were conducted on both the ewes and lambs during wk 2, 4 and 8 of lactation. Nitrogen balance, N digested and the portion of digested N retained were greater (P less than .01) with the MP diet. Nitrogen retention and serum urea-N values were lower for the ewes nursing T lambs. Plasma beta-hydroxybutyrate and serum glucose values were lower (P less than .01) for ewes fed the LP diet, and certain plasma amino acids and the ketogenic amino acids were lower with the LP diet. Insulin increased (P less than .01) with time throughout lactation. Triiodothyronine (T3) concentrations were higher (P less than .01) in ewes nursing T lambs. Thyroxine (T4) was greater (P less than .04) with the LP diet and greater (P less than .01) for ewes nursing T lambs. The T4:T3 ratio was lower (P less than .02) in the ewes consuming LP. The portion of the ewe's retained N used for milk synthesis was lower (P less than .01) with the MP diet. Ewes fed LP and nursing T lambs utilized all of their retained N plus a portion of their body protein reserves for milk production by the 2nd wk of lactation. Body weights of creep-fed lambs were not changed by protein content of the ewe's diet.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.