L-selenomethionine Increases Breast Selenium Deposition in Broilers

A University of Georgia trial compared Nutrilock® SelenoSure™, a hydroxy-selenomethionine analog and sodium selenite at 0.3 ppm added selenium in broilers through 21 days of age.

Added dietary selenium is capped at 0.3 ppm. Within that ceiling, selenium sources can differ substantially in the chemical form of Se delivered and the metabolic route required before that selenium can enter tissue protein.

L-selenomethionine (L-Se-Met) is absorbed and handled like methionine and can be incorporated non-specifically into body proteins, forming a tissue selenium reserve that can later be mobilized through normal protein turnover. Inorganic selenium instead enters the selenide pool for selenoprotein synthesis or excretion. The hydroxy-selenomethionine analog (OH-Se-Met) can also contribute to the tissue SeMet pool, but must first undergo metabolic conversion before becoming L-Se-Met.

Commercial organic selenium sources therefore are not chemically interchangeable. Selenium yeast contains a variable mixture of selenium species, while OH-Se-Met provides a consistent organic precursor to L-Se-Met. Direct-fed L-Se-Met supplies the amino acid itself.

Previous dose-response research reported statistically similar tissue selenium deposition from L-Se-Met and OH-Se-Met across several supplemental Se concentrations. The present study was conducted to test that comparison directly under a commercially relevant 0.3 ppm added-Se program and a moderate heat-stress challenge.

In a 336-bird University of Georgia study, sodium selenite, OH-Se-Met and direct-fed L-Se-Met were each formulated to provide 0.3 ppm of added Se from 0 to 21 days of age. No significant differences in live performance were detected among sources. Breast selenium at D21, however, separated into three distinct statistical groups: Sodium selenite 0.590 C < OH-Se-Met 1.104 B < SelenoSure™ 1.410 A µg/g (P < 0.0001).

At equal formulated supplemental Se, OH-Se-Met deposited 22% less selenium in breast tissue than direct-fed L-Se-Met, while sodium selenite deposited 58% less.

These results demonstrate that, under the conditions of this experiment, supplying an OH-Se-Met precursor and supplying L-Se-Met directly did not result in the same breast selenium deposition.

Selenium is an essential trace mineral with critical roles in antioxidant defense, thyroid metabolism and immune function, and it acts synergistically with vitamin E.

In monogastric diets, supplemental selenium is commonly provided through four commercial strategies:

These sources ultimately supply selenium, but they do not enter metabolism in the same chemical form.

Inorganic selenium is reduced toward the common selenide pool and is utilized primarily for selenoprotein synthesis or excretion. It has limited capacity for non-specific incorporation into body protein.

L-Se-Met, by contrast, is absorbed and handled through the methionine pool. Because it can substitute non-specifically for methionine during protein synthesis, L-Se-Met may be incorporated into structural and storage proteins. This creates a tissue selenium reservoir that can subsequently be mobilized as those proteins turn over.

OH-Se-Met can ultimately contribute to this same tissue pool, but it is supplied as a precursor rather than as L-Se-Met itself and therefore requires metabolic conversion prior to incorporation as SeMet.

KEY POINT: At a fixed added-Se concentration, selenium sources differ not simply by whether they are classified as “organic,” but by the selenium species supplied and the metabolic pathway required for that selenium to reach tissue protein.

The important distinction is therefore between direct delivery of L-Se-Met and routes that must first supply, release or generate L-Se-Met before selenium can be incorporated non-specifically into tissue protein.

Selenium yeasts were developed to increase delivery of organic selenium, but selenium yeast is not a single selenium compound.

Speciation of 13 fresh commercial selenium-yeast samples found that L-Se-Met averaged 55.8% of total Se, with a range of 19.0–71.8%. SeCys averaged 3.8%, elemental selenium ranged from 3.6–51.8%, and an “other/unidentified” fraction averaged 26.3%.

Across these samples, elemental selenium was strongly inversely associated with L-Se-Met content. This relationship is consistent with differences in how selenium is metabolized during yeast production, including diversion of selenium toward elemental Se under conditions in which the yeast must manage excess selenium, rather than incorporation into L-Se-Met.

The practical implication is not that selenium yeast is ineffective. Rather, total selenium concentration does not tell us how much L-Se-Met a yeast product actually supplies, and that proportion may vary substantially among products and lots.

If non-SeMet organic selenium contributed to muscle deposition in the same manner as SeMet, SeCys would be an obvious candidate.

Published work indicates otherwise.

Supplemental SeCys produced a muscle selenium response similar to sodium selenite, and additional SeCys supplied with selenium yeast did not increase tissue selenium deposition to the degree observed when the SeMet content of the source increased.

These observations support the established metabolic distinction: dietary SeCys is catabolized toward the common selenide pool rather than being incorporated non-specifically into tissue protein in the same manner as L-Se-Met.

Across published comparisons, selenium yeasts with a greater SeMet fraction have generally produced greater muscle selenium deposition.

An earlier broiler study likewise ranked muscle Se: Sodium selenite < selenium yeast < OH-Se-Met.

More recent work comparing selenium yeasts containing differing proportions of SeMet again demonstrated that tissue deposition increased as the dietary contribution of SeMet increased.

Selected treatments from De Marco et al. (2021) provide another useful way to examine this relationship.

Table 2: Muscle selenium relative to L-Se-Met or precursor supplied

NC = negative control. Sodium selenite and selenium yeast treatments shown above received 0.30 ppm added Se. The L-Se-Met and OH-Se-Met treatments shown received 0.15 ppm added Se. Values were selected from De Marco et al. (2021) to examine tissue deposition relative to the amount of L-Se-Met or precursor supplied.

When expressed relative to the dietary SeMet or SeMet-precursor contribution, the four organic treatments fall within a relatively narrow tissue:diet range of 4.31–4.67 despite differences in source and treatment structure.

This relationship supports the broader observation that muscle selenium deposition closely tracks the amount of dietary selenium supplied through the SeMet pathway.

The OH-Se-Met analog, hydroxy-4-methylselenobutanoic acid (HMSeBA), represented an important advance in selenium supplementation because it provides a consistent organic SeMet precursor and has demonstrated improvements in tissue selenium deposition relative to inorganic selenium.

OH-Se-Met, however, is not L-Se-Met.

It must undergo metabolic conversion before reaching the L-Se-Met pool and becoming available for incorporation into tissue protein.

The analogous sulfur methionine system provides evidence that hydroxy-methionine analogs and L-methionine are not metabolically identical. Baker’s compiled utilization data, for example, report lower relative utilization of DL-OH-Met than L-Met in chicks.

Those sulfur-amino-acid data demonstrate that the conversion step can have biological consequences, but they should not be interpreted as establishing a fixed conversion efficiency for OH-Se-Met itself.

Previous dose-response work by De Marco et al. (2021) found L-Se-Met and OH-Se-Met tissue deposition to be statistically similar at 0.15, 0.30, 0.45 and 0.60 ppm supplemental Se.

At 0.15 ppm, however, breast Se was numerically greater with L-Se-Met than OH-Se-Met (0.80 vs. 0.75 mg/kg DM). Although this difference was not statistically significant, it raised the question of whether the numerical separation reflected a biological consequence of supplying L-Se-Met directly rather than through the OH-Se-Met analog, or simply normal analytical and experimental variation.

Given this numerical observation and the requirement for OH-Se-Met to undergo conversion before entering the L-Se-Met pool, does supplying OH-Se-Met produce a measurable difference in tissue selenium deposition when compared directly with L-Se-Met?

The present trial was designed to test that question at the commercially relevant 0.3 ppm added-Se level under a moderate heat-stress challenge.

Primary: To compare a 100% L-selenomethionine source (SelenoSure^™), sodium selenite and an OH-Se-Met analog in terms of selenium status in broilers from 0 to 21 days of age.

Secondary I: To determine whether a practical difference exists between OH-Se-Met and direct-fed L-Se-Met at a major selenium deposition site, the pectoralis major.

Secondary II: To evaluate whether selenium source was associated with differences in body weight, body-weight gain, feed intake, feed conversion or mortality through 21 days.

Five hundred Ross 708 male chicks were obtained from a commercial hatchery in Georgia and sorted into 2-g weight categories.

Extreme weights of less than 35 g or greater than 49 g were excluded, and starting cage mean weights were maintained within a 10-g variance.

A total of 336 broilers were placed into 48 cages at 7 birds per cage.

Three treatments were evaluated in a single feeding phase. Each treatment was formulated to provide 0.300 ppm of ADDED selenium from its respective experimental source.

Birds were fed a single starter mash diet ad libitum from D0 through D21.

Experimental selenium sources were incorporated into trace mineral premixes included at 0.075% of complete feed and combined with a common basal diet comprising the remaining 99.925%.

Each experimental trace mineral premix was first mixed with a subset of the common basal diet in a standing Hobart mixer for 15 minutes. Complete treatments were subsequently mixed in a 500-lb Davis mixer for 12 minutes.

The trace mineral premix provided:

• 125 ppm Cu from hydroxychloride
• 40 ppm Zn from hydroxychloride
• 40 ppm Mn from hydroxychloride
• 20 ppm Fe from sulfate
• 3.00 ppm I from calcium iodate
• 0.300 ppm formulated ADDED Se from the respective experimental selenium source

Diets supplied 36 IU/lb vitamin E.

The common basal diet contained 0.174 ppm Se. Experimental trace mineral premixes were formulated to provide 0.300 ppm of ADDED Se, while analyzed selenium supplied through the trace mineral premixes was 0.261 ppm on an as-is basis (CVAS).

The formulated supplemental selenium target and analytical result are reported separately to distinguish intended dietary supplementation from analyzed selenium recovery.

Data were subjected to ANOVA according to the General Linear Model, with treatment and block included as factors.

Tukey’s multiple-comparison procedure was used to detect significant differences among dietary treatments.

Differences were considered significant at P < 0.05.

All statistical procedures were completed using Minitab, Release 19.

No statistically significant differences among selenium sources were detected for body weight, body-weight gain, feed intake or mortality-adjusted FCR through 21 days of age.

Under these experimental conditions, live performance did not differ among selenium sources.

Breast selenium concentration at 21 days differed markedly among selenium sources (P < 0.0001) and separated into three distinct statistical groups:

Sodium selenite (0.590 C) < OH-Se-Met (1.104 B) < L-Se-Met / SelenoSure™ (1.410 A) µg/g

Relative to SelenoSure™, the OH-Se-Met analog deposited 22% less selenium in breast tissue at the same formulated 0.300 ppm added-Se concentration, while sodium selenite deposited 58% less.

Expressed in the opposite direction, direct-fed L-Se-Met increased breast selenium by 28% relative to OH-Se-Met and 139% relative to sodium selenite.

The live-performance and tissue-deposition results should be considered together, but they measure different biological outcomes.

No significant differences were detected in BW, BWG, feed intake or mortality-adjusted FCR.

Breast selenium provided a different response.

Sodium selenite produced the lowest tissue selenium concentration, consistent with its metabolism through the inorganic selenium pool and lack of direct incorporation into general tissue protein through the methionine pathway.

OH-Se-Met produced substantially greater breast selenium than sodium selenite. This confirms that the hydroxy analog can effectively contribute selenium toward tissue deposition.

Direct-fed L-Se-Met, however, produced significantly greater breast selenium than OH-Se-Met at the same formulated supplemental selenium concentration.

This distinction is particularly notable because previous published dose-response work reported statistical similarity between L-Se-Met and OH-Se-Met across multiple dietary selenium concentrations.

The present trial therefore did not reproduce equivalence in tissue deposition between L-Se-Met and OH-Se-Met.

Mechanistically, direct-fed L-Se-Met and OH-Se-Met reach the tissue SeMet pool by different routes. Direct-fed L-Se-Met enters the methionine pool as L-Se-Met itself, whereas OH-Se-Met must first undergo metabolic conversion.

The current experiment demonstrates a biological difference between those two supplementation strategies but does not independently establish the mechanism responsible for that difference.

What can be concluded directly from the present data is more straightforward:

At equivalent levels of supplemental Se, direct-fed L-Se-Met resulted in significantly greater breast selenium deposition than OH-Se0Met at 21 days of age.

Commercial selenium programs are commonly compared on the basis of total added selenium.

Because added dietary selenium is capped at 0.3 ppm, total selenium alone does not describe the chemical form supplied to the bird.

Programs can differ in:

The table below therefore describes what is supplied in the feed rather than assigning OH-Se-Met a fixed biological conversion percentage.

*Pricing is illustrative, expressed in $/ton of complete feed, and should be confirmed against current quotations. **Example yeast calculations assume 63% of total selenium is supplied as L-Se-Met. This commercial-program assumption is separate from the 55.8% mean reported across the 13 commercial selenium yeasts characterized by Hachemi et al. (2023).

This comparison deliberately separates directly supplied L-Se-Met from OH-Se-Met precursor rather than assuming a fixed percentage conversion of OH-Se-Met to L-Se-Met.

The biological comparison is instead provided by the feeding trial itself: when both sources were formulated to supply 0.300 ppm added Se, direct-fed L-Se-Met produced significantly greater breast selenium deposition than OH-Se-Met.

• No statistically significant differences in body weight, body-weight gain, feed intake or mortality-adjusted FCR were detected among sodium selenite, OH-Se-Met and SelenoSure^™ through 21 days of age.
• Breast selenium concentration separated into three distinct statistical groups (P < 0.0001):  Sodium selenite  <  OH-Se-Met  <  L-Se-Met

• OH-Se-Met produced substantially greater tissue selenium deposition than sodium selenite, demonstrating effective contribution of the hydroxy analog to the tissue selenium pool.
• Direct-fed L-Se-Met produced 28% greater breast selenium concentration than OH-Se-Met at the same formulated 0.300 ppm added-Se concentration.
• Previous published work reported statistical similarity between L-Se-Met and OH-Se-Met under other experimental conditions. The present study did not reproduce that result.
• The present experiment establishes a difference in tissue deposition but does not by itself establish the biochemical mechanism responsible for that difference.
• Direct-fed L-Se-Met supplies the dietary molecule that can enter the methionine pool directly, without requiring prior conversion from an analog.

Baker, D.H. (2006). Comparative species utilization and toxicity of sulfur amino acids. The Journal of Nutrition, 136(6 Suppl), 1670S–1675S. See also Baker et al. (1982, 1980, 1975).

Briens, M., Mercier, Y., Rouffineau, F., Vacchina, V., & Geraert, P.-A. (2013). Comparative study of a new organic selenium source v. seleno-yeast and mineral selenium sources on muscle selenium enrichment and selenium digestibility in broiler chickens. British Journal of Nutrition, 110(4), 617–624.

De Marco, M., Conjat, A.-S., Briens, M., Hachemi, M.A., & Geraert, P.-A. (2021). Bio-efficacy of organic selenium compounds in broiler chickens. Italian Journal of Animal Science, 20(1), 514–525.

Hachemi, M.A., Cardoso, D., De Marco, M., Geraert, P.-A., & Briens, M. (2023). Inorganic and organic selenium speciation of seleno-yeasts used as feed additives: new insights from elemental selenium determination. Biological Trace Element Research, 201, 5839–5847.

University of Georgia broiler trial, 0–21 D. Data on file, Chemlock Nutrition, Cincinnati, OH.