HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Free Via Open Access Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in Web of Science Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Qiao, H. Y. Articles by Classen, H. L. Search for Related Content PubMed Articles by Qiao, H. Y. Articles by Classen, H. L.

Nutritional and Physiological Effects of Dietary Sinapic Acid (4-Hydroxy-3,5-Dimethoxy-Cinnamic Acid) in Broiler Chickens and its Metabolism in the Digestive Tract

Department of Animal and Poultry Science, University of Saskatchewan, 51 Campus Drive, Saskatoon, Saskatchewan, Canada, S7N 5A8

¹ Corresponding author: hank.classen{at}usask.ca

	ABSTRACT

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
Sinapic acid (SA) is a major free phenolic acid in rapeseed meal, with the majority found in the esterified form of sinapine. Two experiments were conducted to delineate the effect of dietary SA on broiler chickens, in terms of performance, toxicity, and nutrient digestibility. In the first experiment, 80 male broiler chicks were randomly assigned to 5 diets adequate in all nutrients and containing 0, 0.05, 0.10, 0.15, or 0.20% dietary SA. Performance from 0 to 18 d of age and the relative size of all the internal organs and intestines were not affected (all P > 0.05) by dietary treatment. In addition, dietary SA had no effect (P > 0.05) on the serum activity of creatine kinase and lactate dehydrogenase, which indicated that there was no damage to skeletal muscle, heart muscle, liver, kidneys, or brain. The objectives of the second experiment were to investigate the effect of SA on nutrient retention and to study the retention of SA in the digestive tract. Male broiler chicks (96) were randomly assigned into 4 treatments containing dietary SA at 0, 0.025, 0.05, and 0.10%. Dietary SA at the 0.025% level increased feed intake compared with control (P < 0.05). Regression analysis indicated a quadratic response for both weight gain and feed intake (P < 0.05) as SA increased in the diet. Again, dietary SA did not affect the relative weights of bursa of Fabricius, liver, kidney, or digestive tract. Nitrogen-corrected AME and protein digestibility were not affected by SA level. A negative linear relationship was found between dietary SA level and apparent ileal digestibility of Met, Thr, Ser, Pro, Gly, Ala, and Phe. Sinapic acid disappearance in the ileum was above 97% for all SA levels, whereas apparent SA retention in excreta ranged from 64 to 79%. Sinapic acid at dietary levels investigated in this research is apparently not toxic to broiler chickens but may have a negative effect on amino acid digestibility at higher levels.

Key Words: sinapic acid • rapeseed • broiler • nutrient • metabolism

	INTRODUCTION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
Sinapic acid (SA, 4-hydroxy-3,5-dimethoxy-cinnamic acid) is the predominant free phenolic acid found in rape-seed. Sinapic acid constitutes up to 15% of total phenolics in rapeseed meal (RSM) and up to 99% of phenolic acids released from esters and glucosides in rapeseed flours (Krygier et al., 1982). It can be estimated that the free SA content in RSM may range from 0.05 to 0.40% or higher on a DM basis depending on the variety, growing location and conditions, and processing method (Krygier et al., 1982; Shahidi and Naczk, 1992; Qiao, 2002). A large proportion of SA is found as a portion of the compound sinapine (SNP). Sinapine is the major phenolic compound in RSM and is comprised of SA esterified to choline. As with SNP, little research has been done on SA in RSM from either a chemical or biological standpoint.

It has long been recognized that compounds in the 4-hydroxy-3,5-dimethoxy-phenyl group occur widely in dietary material of plant origin. Dietary constituents of this type may give rise to metabolites possessing undesirable psychopharmacological properties, such as in schizophrenic individuals in which abnormalities of methylation may exist (Kety, 1965). In animal nutrition, it has been reported that phenolic compounds in RSM, mainly SNP and SA, may contribute to the dark color, bitter taste, and astringency of the meal (Sosulski et al., 1977; Sosulski, 1979; Shahidi and Naczk, 1995; Naczk et al., 1998). Therefore, they are thought to be responsible for palatability problems associated with feeding RSM to monogastric animals (Josefsson and Uppstrom, 1976; Lee et al., 1984). They are also frequently reported to be responsible for the deleterious properties of protein products derived from rapeseed (Rutkowski and Kozlowska, 1979; Rubino et al., 1996).

In vitro studies have demonstrated phenolic compounds or their derived products, or both, have the potential to form complexes with protein and digestive enzymes (Wada et al., 1969; Ismail et al., 1981; Naczk et al., 1998). It has been speculated that the presence of phenolic compounds may lower the nutritional value of rapeseed products by this mechanism (Ismail et al., 1981; Lee et al., 1984, Kozlowska et al., 1990), although in vivo evidence is lacking.

Sinapic acid, as an organic acid and a member of 4-hydroxy-cinnamic acids, may also be biologically active. Sinapic acid has also been shown to have strong antioxidative (Nowak et al., 1992; Wanasundara et al., 1996) and antibacterial activity in vitro (Nowak et al., 1992; Tesaki et al., 1998).

Although the concentration of SA in free form in RSM is relatively low, there is the potential for larger amounts of SA to be released from SNP in the digestive tract of animals (Qiao and Classen, 2003). This suggests that specific knowledge on the nutritional and toxicological role of SA in animal feeding is required. Therefore, 2 experiments were conducted to study the effect of dietary SA on broiler chickens. The objectives of the first experiment were to investigate nutritional and toxicological effects of SA. The second experiment was conducted to confirm the results of the first trial, to investigate the effect of SA on nutrient digestibility, and to study the metabolism of SA in the digestive tract of broilers.

	MATERIALS AND METHODS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
Experimental protocols were approved by the Animal Care Committee of the University of Saskatchewan and were performed in accordance with recommendations of the Canadian Council on Animal Care (1993) as specified in the Guide to the Care and Use of Experimental Animals.

Birds and Diets

Experiment 1. Five treatments consisted of maize (Zea mays)-soybean meal diets supplemented with graded levels of dietary SA (0, 0.05, 0.10, 0.15, and 0.20%). Sinapic acid addition was equivalent to the SA profiles of SNP when RSM is added at 7.5, 15, 22.5, and 30% in the formula diet and the SNP content in RSM is 1%. It can be speculated that the dietary SA level at 0.05% is equivalent or higher than the free-SA content of a diet containing 30% RSM. Each diet was replicated 4 times with 4 birds per replication. A total of 80 one-day-old male broiler chicks (Peterson x Hubbard) were randomly assigned to experimental units.

Experiment 2. Four treatments were based on a maize-soybean meal diet with graded levels of dietary SA (0, 0.025, 0.05, and 0.10%). Ninety-six 1-d-old male Peterson x Hubbard chicks were randomly assigned to replicate groups of 6 birds each, with 4 replicates per dietary treatment.

Broilers were housed in battery brooders. Temperature was maintained in accordance with standard brooding management, and light was provided for 23 h and 16 h from 0 to 5 and 5 to 18 d of age, respectively. Feed, in mash form, and water were provided for ad libitum consumption. Sinapic acid was purchased from Sigma Chemical Co. (St. Louis, MO) with a purity of 98% (GC grade, lot 128H3485, light yellow or milky color, dry powder) and was diluted with maize before feed manufacture. Diets were formulated to be isoenergetic and isonitrogenous and either meet or exceed the nutrient requirements of broiler chicks as recommended by the NRC (1994). Diet composition and nutrient levels are shown in Table 1.

Experiment 1. Weight gain and feed consumption for each pen were measured at 7, 14, and 18 d of age, whereas mortality was recorded and weighed daily. At the end of 18 d, the birds were individually weighed, blood was sampled to provide serum for analysis of creatine kinase (CK) and lactate dehydrogenase (LD), the birds were killed by lethal injection with T-61 Euthanasia solution (Hoechst, Somerville, NJ), and internal organs (bursa of Fabricius, heart, kidney, liver, spleen, pancreas, proventriculus, gizzard) and intestines (duodenum, jejunum, ileum, and ceca) were removed and measured. For each section of the digestive tract, both full and empty weights were measured. The major internal organs were weighed to determine if SA was toxic to broiler chickens, because the liver is involved in the detoxification process, the kidneys are involved in excretion of toxic metabolites, and bursa of Fabricius is an indicator of bird immune status.

Experiment 2. Production variables were measured from 0 to 18 d of age. Excreta were collected for each pen from 16 to 18 d of age. At the end of 18 d, the birds were individually weighed and euthanized by chemical agent (T-61). All internal organs and digestive tracts were removed and examined, and the bursa of Fabricius, liver, kidney, full and empty ileum and ceca were measured. Distal ileal (a section halfway between Meckel’s diverticulum and 2 cm anterior to the ileal-cecal junction) and cecal contents were collected from each bird and pooled within a pen and immediately frozen at –20°C until further analysis.

Sample Analysis

Creatine kinase and LD activity were measured in serum at 340 nm by spectrophotometry using Anthos Reader 2001 (Anthos Labtec Instruments, A-5022, Salzburg, Austria) according to the Sigma diagnostics kits for CK and LD (Sigma Chemical Co.). Acid insoluble ash (AIA) was used as an indigestible marker for the determination of AME, apparent digestibility of protein (ileal and excreta), and SA retention. The AIA was determined by using the procedure of Vogtmann et al. (1975). Gross energy was measured using an oxygen bomb calorimeter (model 1281, Parr Instruments, Moline, IL). Crude N content was determined by combustion method (984.13) of AOAC International (1995) using a Leco FP-528 protein analyzer (model no. 601-500-100, Leco Corporation, St. Joseph MI). Amino acids were determined by using an amino acid analyzer (Beckman System Gold, Beckman Instruments Inc., Palo Alto, CA) based upon the sodium metabisulfite method (Llames and Fontaine, 1994). The apparent retention of nutrient and SA was based on the assay of nutrient, SA and AIA in feed, excreta, and ileal contents.

The following calculations were used to determine the diet AME, N retention, SA retention, and amino acid digestibility:

where GE = gross energy [kcal per kg of sample (diet, excreta, or ileal digesta)]; marker = concentration of AIA.

where marker = concentration of AIA.

where marker = concentration of AIA.

where (AA/AIA)_d = ratio of amino acid to AIA in diet and (AA/AIA)_i = ratio of amino acid to AIA in ileal digesta.

Analysis of SA in Feed, Excreta, and Ileal Samples

For sample preparation, samples were ground to 0.5 mm and added (feed and excreta: 50 mg; ileal sample: 0.15 mg) to a 15-mL screw-top test tube containing 5 mL of 70% methanol (acidified with 1% HCl). The contents of the tube were mixed well before the tube was capped, then the contents were heated at 75°C in a water bath for 20 min. Another 5 mL of 70% acidified methanol was added to the cooled extract, and the extract was centrifuged (1,000 x g, 4°C, 10 min). The supernatant was transferred to HPLC vials for analysis. The determination of SA was conducted on a HPLC (Beckman System Gold, Beckman Instruments Inc.) using a reversed-phase column (PRP-1, 150 x 4.1 mm, i.d. 5 µm, Hamilton Company, Reno, Nevada) and a fluorescence detection method (RF 551 spectroflurometric detector, Shimadazu Scientific Instruments Inc. Columbia, MD). The excitation and emission wavelengths of SA were determined as 280 nm and 428 nm previously. The mobile phase was isocratic, based on 6% methanol solution with 20 mmol of K₂HPO₄ as basic buffer (buffered at pH 9.5 or 9.0). The SA content was analyzed in the diets of experiment 2 only.

Statistical Analyses

Data for tissue weights, lengths, or both, were based on relative values of organ or intestinal weight (length) value/BW. All data were subjected to 1-way ANOVA according to GLM procedure and a priori contrast, as well as the regression analysis by the SAS program (SAS Institute, 1999). Differences were considered significant when P < 0.05, unless otherwise stated.

	RESULTS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
Experiment 1

Performance and Tissue Measurements. There were no differences (P > 0.05) among dietary SA treatments with respect to the BW gain, feed consumption, and feed efficiency (gain:feed ratio; Table 2). No differences were observed among the 5 treatments in the relative weight of the bursa of Fabricius, heart, liver, kidney, spleen, or pancreas (Table 2). Similarly, treatment did not affect relative weight of the proventriculus and gizzard and the length and full and empty weights of duodenum, jejunum, ileum, or ceca (Table 2 and 3). The empty ileum weight of the 0.15% SA treatment was heavier than other SA treatments (P < 0.05) but did not differ from the control (Table 3).

Experiment 2

Performance and Tissue Measurements. A quadratic relationship was demonstrated between dietary SA and weight gain (P = 0.03; Table 4). Weight gain was highest at the lowest level of SA inclusion (0.025%) and declined to near control values for the highest level of SA inclusion (0.1%). Feed intake was similarly affected by dietary SA as indicated by ANOVA (P = 0.02) and regression analysis (quadratic P = 0.008). Feed intake for the 0.025% level was higher than both the control and the 0.1% level, which did not differ. Gain-to-feed ratio was not affected by dietary treatment. There were no differences among treatments in the relative weight of the bursa of Fabricicus, kidney and liver, and the relative weight and length of the full and empty ileum (Table 4). Cecal length and full weight were not affected by dietary SA, but empty cecal weight decreased in a linear fashion with increasing levels of SA (linear regression, P < 0.05).

The AME_n, apparent ileal protein retention, and apparent N retention in excreta were not significantly affected by dietary SA level (Table 5). Sinapic acid disappeared in high proportion before the terminal ileum as shown by apparent ileal retention values between 97.0 and 97.8% for the 3 SA diets. Apparent SA retention in the excreta ranged from 63.8 to 79.3% for the 3 dietary SA treatments (P < 0.001), and the absolute value varied with treatment (Table 5). The lowest level of dietary SA at 0.025% had the highest value for SA retention in the excreta. There was no SA found in the cecal digesta samples of all treatments with dietary SA inclusion (data not shown).

	DISCUSSION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

The present findings are in agreement with that of Griffiths (1969), who orally administered SA (200 mg) to rats (250 g of BW) and observed no effect of this phenolic compound on growth performance.

A potential beneficial effect of dietary SA, as indicated by growth rate and feed intake at low levels of dietary SA treatment in experiment 2, may be associated with the antioxidant and antibacterial activity of SA and related plant phenolics. For example, ferulic acid has been claimed to lessen the effects of chemo- and radiotherapy of carcinomas by increasing the natural immune defense (Graf, 1992). Other beneficial effects of ferulic acid include strong antiinflammatory properties in a rat paw edema model, inhibition of chemically induced carcinogenesis in rats, and tumor promotion in mouse skin (Graf, 1992). Work with ferulic acid is of interest because of the similarity in structures of ferulic acid and SA. Ferulic acid is a precursor in SA synthesis, and both are derived from the phenylpropanoid pathway (Tesaki et al., 1998). They both have a hydroxy group attached to the 4-position of the benzene ring, a methoxy group at the 5-position, and a double bond between the same carbons of the side chain. Therefore, they may have similar biological effects when consumed. Sinapic acid has been shown to have strong antioxidant activity in vitro (Nowak et al., 1992). Also similar to ferulic acid is the more recent in vitro demonstration that SA has antibacterial activity (Tesaki et al., 1998; Hua et al., 1999). It is of interest that empty cecal weight was reduced in response to increasing dietary SA in 1 of the 2 experiments in the present study. This is similar to the response previously noted for SNP (Qiao and Classen, 2003).

Sinapic acid was nearly absent from the terminal end of the ileum, and, as a consequence, ileal SA disappearance values were very high (97.0 to 97.8%). In contrast, apparent SA retention values in the excreta were much lower (63.8 to 79.3%). These data suggest that SA is likely absorbed before the terminal ileum and that at least a portion of the SA was excreted intact via the kidney. The latter is in agreement with a report on SA metabolism in rats that demonstrated the excretion of a portion of the intact form of SA in urine (Griffiths, 1969). In addition, several other phenolic metabolites derived from SA were also found in the urine in that study. Research with other phenolic acids (cinnamic, caffeic, and ferulic acid) has also shown substantial absorption in the small intestine (Jung and Fahey, 1983; Wolffram et al., 1995; Olthof et al., 2001). With respect to excretion, it has been suggested that ingestion of plant phenolics results in a considerable increase in urinary excretion of phenolics and that most of the absorbed phenolics are metabolically transformed before being excreted (Martin, 1982; Silanikove and Brosh, 1989; Arin et al., 1992). Other studies have also indicated that intestinal microflora can modify phenolic compounds in the digestive tract of rats, more likely in the lower gut. Intestinal bacteria may modify SA by various reactions including dehydroxylation, demethoxylation, and reduction reactions (Griffiths, 1969; Jung and Fahey, 1983). Therefore, there is the possibility that gut microorganisms, especially in the hindgut, modified a portion of dietary SA in the current study. The effect of SA on empty cecal weight in experiment 2 and the failure to find SA in the ceca of birds fed either SA or SNP support this point. A comprehensive study capable of monitoring gut and postabsorption modification of SA and identification of the resulting compounds is required to fully understand in vivo SA metabolism and its effect on the host animal.

Because SA is capable of binding protein in vitro (Kozlowska et al., 1990), it was of interest to see if dietary SA affected in vivo nutrient retention. In experiment 2, the digestibility of several amino acids similarly decreased in a linear fashion in response to increased diet SA. Nitrogen retention in excreta was not affected by diet SA. This information plus the increase in growth rate (7.5%) associated with low level (0.025%) of dietary SA suggest that there may be both negative and positive effects associated with feeding SA to broiler chickens, with the response being dose-dependent. The effect of dietary SA on nutrient retention requires confirmation. If confirmed, additional research is required to establish whether they relate to pre- and postabsorptive effects of SA.

	ACKNOWLEDGMENTS

 
This research was supported by the Saskatchewan Agriculture, Food and Rural Revitalization Agricultural Development Fund and a Saskatchewan Canola Development Commission Scholarship. We wish to acknowledge the contribution of the Poultry Research Group staff at the University of Saskatchewan for technical assistance with animal trials and laboratory analysis.

Received for publication August 24, 2007. Accepted for publication January 5, 2008.

	REFERENCES

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
AOAC International. 1995. Official Methods of Analysis of AOAC International. 16th ed. AOAC Int., Arlington, VA.

Arin, M. J., M. T. Diez, and J. A. Resines. 1992. Rapid and simple method for the determination of urinary benzoic and phenylacetic acids and their glycine conjugates in ruminants by reversed-phase high-performance liquid chromatography. J. Chromatogr. 582:13–18.[CrossRef][Web of Science][Medline]

Canadian Council on Animal Care. 1993. Guide to the Care and Use of Experimental Animals. Vol. 1. Can. Counc. Anim. Care, Ottawa, Ontario, Canada.

Graf, E. 1992. Antioxidant potential of ferulic acid. Free Rad. Biol. Med. 13:435–448.[CrossRef][Web of Science][Medline]

Griffiths, L. A. 1969. Metabolism of sinapic acid and related compounds in the rat. Biochem. J. 113:603–609.[Web of Science][Medline]

Hua, S. S., O. K. Grosjean, and J. L. Baker. 1999. Inhibition of aflatoxin biosynthesis by phenolic compounds. Lett. Appl. Microbiol. 29:289–291.[CrossRef][Web of Science][Medline]

Ismail, F., M. Vaisey-Genser, and B. Fyfe. 1981. Bitterness and astringency of sinapine and its components. J. Food Sci. 46:1241–1244.[CrossRef][Web of Science]

Josefsson, E., and B. Uppstrom. 1976. Influence of sinapine and p-hydroxybenzyl-glucosinolate on the nutritional value of rapeseed and white mustard meals. J. Sci. Food Agric. 27:438–442.[CrossRef][Web of Science][Medline]

Jung, H. G., and G. C. Fahey Jr. 1983. Effects of phenolic monomers on rat performance and metabolism. J. Nutr. 113:546–549.[Abstract/Free Full Text]

Kety, S. S. 1965. Biochemistry and mental function. Nature 208:1252–1257.[CrossRef][Medline]

Kozlowska, H., M. Naczk, F. Shahidi, and R. Zadernowski. 1990. Phenolic acids and tannins in rapeseed and canola. Pages 193–210 in Canola and Rapeseed: Production, Chemistry, Nutrition and Processing Technology. F. Shahidi, ed. AVI Book, New York, NY.

Krygier, K., F. Sosulski, and L. Hogge. 1982. Free, esterified and insoluble-bound phenolic acids. 2. Composition of phenolic acids in rapeseed flour and hulls. J. Agric. Food Chem. 30:334–336.[CrossRef][Web of Science]

Lee, P. A., S. Pittam, and R. Hill. 1984. The voluntary food intake by growing pigs of diets containing ‘treated’ rapeseed meals or extracts of rapeseed meal. Br. J. Nutr. 52:159–164.[CrossRef][Web of Science][Medline]

Llames, C. R., and J. Fontaine. 1994. Determination of amino acids in feeds: Collaborative study. J. AOAC Int. 77:1362–1402.[Web of Science]

Martin, A. K. 1982. The origin of urinary aromatic compounds excreted by ruminants. 2. The metabolism of phenolic cinnamic acids to benzoic acid. Br. J. Nutr. 47:155–164.[CrossRef][Web of Science][Medline]

Naczk, M., R. Amarowicz, A. Sullivan, and F. Shahidi. 1998. Current research developments on polyphenolics of rape-seed/canola: A review. Food Chem. 62:489–502.[CrossRef]

Nowak, H., K. Kujawa, R. Zadernowski, B. Roczniak, and H. Kozlowska. 1992. Antioxidative and bactericidal properties of phenolic compounds in rapeseeds. Fat Sci. Technol. 94:149–152.

NRC. 1994. Nutrient Requirement of Chicken. 9th ed. Natl. Acad. Press, Washington, DC.

Olthof, M. R., P. C. H. Hollman, and M. B. Katan. 2001. Chlorogenic acid and caffeic acid are absorbed in humans. J. Nutr. 131:66–71.[Abstract/Free Full Text]

Qiao, H. 2002. Nutritional, physiological and metabolic effects of rapeseed meal simple phenolics in broiler chickens. PhD Diss. Univ. Saskatchewan, Saskatoon, Canada.

Qiao, H., and H. L. Classen. 2003. Nutritional and physiological effects of rapeseed meal sinapine in broiler chickens and its metabolism in the digestive tract. J. Sci. Food Agric. 83:1430–1438.[CrossRef][Web of Science]

Rubino, M. I., S. D. Arntfield, C. A. Nadon, and A. Bernatsky. 1996. Phenolic protein interactions in relation to the gelation properties of canola protein. Food Res. Int. 29:653–659.[CrossRef]

Rutkowski, A., and H. Kozlowska. 1979. Chemical constituents and protein food processing of rapeseed. J. Am. Oil Chem. Soc. 56:475–477.[CrossRef][Web of Science][Medline]

SAS Institute. 1999. SAS User’s Guide: Statistics. SAS Inst. Inc., Cary, NC.

Shahidi, F., and M. Naczk. 1992. An overview of the phenolics of canola and rapeseed: Chemical, sensory and nutritional significance. J. Am. Oil Chem. Soc. 69:917–924.[CrossRef][Web of Science]

Shahidi, F., and M. Naczk. 1995. Methods of analysis and quantification of phenolic compounds. Pages 20–65 in Food Phenolics: Source, Chemistry, Effects, and Applications. Technomic Publ. Co. Inc., Lancaster, PA.

Silanikove, N., and A. Brosh. 1989. Lignocellulose degradation and subsequent metabolism of lignin fermentation products by the desert black Bedouin goat fed on wheat straw as a single component diet. Br. J. Nutr. 62:509–520.[CrossRef][Web of Science][Medline]

Sosulski, F. 1979. Organoleptic and nutritional effects of phenolic compounds on oilseed protein products: A review. J. Am. Oil Chem. Soc. 56:711–715.[CrossRef][Web of Science]

Sosulski, F., E. S. Humbert, and M. J. Y. Lin. 1977. Rapeseed-supplemented wieners. Can. Inst. Food Sci. Technol. J. 10:9–12.

Tesaki, S., S. Tanabe, H. Ono, E. Fukushi, J. Kawabata, and M. Watanabe. 1998. 4-Hydroxy-3-nitrophenylacetic and sinapic acids as antibacterial compounds from mustard seeds. Biosci. Biotechnol. Biochem. 62:998–1000.[CrossRef]

Vogtmann, H., P. Friter, and A. L. Prabuck. 1975. A new method of determining metabolisability of energy and digestibility of fatty acids in broiler diets. Br. Poult. Sci. 67:641–646.

Wada, S., S. Tomioka, and I. Moriguchi. 1969. Protein bindings. VI. Bindings of phenols to bovine serum albumin. Chem. Pharm. Bull. (Tokyo) 17:320–323.[Medline]

Wanasundara, U., R. Amarowicz, and F. Shahidi. 1996. Partial characterisation of natural antioxidants in canola meal. Food Res. Int. 28:525–530.[CrossRef]

Wolffram, S., T. Weber, B. Grenacher, and E. Scharrer. 1995. A Na⁺ dependent mechanism is involved in mucosal uptake of cinnamic acid across the jejunal brush border in rats. J. Nutr. 125:1300–1308.[Abstract/Free Full Text]

This article has been cited by other articles:

				M. L. Johnson, J. P. Dahiya, A. A. Olkowski, and H. L. Classen The Effect of Dietary Sinapic Acid (4-Hydroxy-3, 5-Dimethoxy-Cinnamic Acid) on Gastrointestinal Tract Microbial Fermentation, Nutrient Utilization, and Egg Quality in Laying Hens Poult. Sci., May 1, 2008; 87(5): 958 - 963. [Abstract] [Full Text] [PDF]

This Article Free Via Open Access Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in Web of Science Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Qiao, H. Y. Articles by Classen, H. L. Search for Related Content PubMed Articles by Qiao, H. Y. Articles by Classen, H. L.