Effect of Dietary C steine Supplements on Canola Meal Toxicity an Altered Hepatic GIuta.thione Metabolism in the Rat1V2


T. K. Smiths and T. M. Bray

ABSTRACT: Experiments were conducted to determine the effects of feeding canola meal Brassica campestris and Brassica napus) on the rat hepatic glutathione detoxification system and whether dietary cysteine supplements might modify such effects. Rats were fed test diets for 14 d. Body weight change, feed consumption, hepatic glutathione concentration, and hepatic glutathione-S-transferase(GSH-S-TIactivities were determined. Weight gain was decreased when canola meal was fed, whereas hepatic glutathione concentrations increased, a s did hepatic GSH-S-T activity. All effects correlated with total glucosinolate concentration in the canola meal. Dietary cysteine supplements, however, did not influence the growth reduction and increased hepatic

glutathione concentrations caused by feeding canola meal. Supplemental cysteine prevented the elevation in hepatic GSH-S-T activity. The elevation in hepatic glutathione concentration caused by canola meals was not a n overcompensation caused by a n initial depletion and therefore reflected a general hepatotoxicity. Feeding supplemental cysteine increased hepatic glutathione levels a t early time intervals and delayed the induction of GSH-S-T caused by canola meal toxicity. There was no beneficial effect of supplemental dietary cysteine in overcoming the toxicity of high levels of canola meal, but supplemental cysteine did modify the canola meal-induced changes in hepatic glutathione metabolism.

Key Words: Glutathione, Rats, Rapeseed Meal, Cysteine, Glucosinolates

J. Anim. Sci. 1992. 70:2510-2515

Introduction The use of canola meal as a protein source in animal diets has been expanded by the development of cultivars containing reduced amounts of glucosinolates and other undesirable components (Bell, 1984). Despite these advances nonruminant animals continue to perform below expectations when canola meal is fed. This is partially attributed to residual glucosinolates. Cruciferous vegetables, such as cabbage, seemingly increase activities of hepatic and intestinal

'These studies were supported by the Ontario Ministry of Agric. and Food and the Nat. Sci. and Eng. Res. Council of Canada. 2The technical assistance of Donald Saunders and Kathy Homonko is gratefully acknowledged. Glucosinolate analysis of canola meals was expertly and kindly conducted by Brian E. Ellis, Dept. of Plant Sci., Univ. of British Columbia. 3To whom correspondence should be addressed. Received July 26, 1991. Accepted March 17, 1992.

xenobiotic-metabolizing enzymes (Whitty and Bjeldanes, 19871, and this effect has been correlated with glucosinolate content (Stoewsand et al., 1986). Glucosinolate hydrolysis products such as allyl isothiocyanate and goitrin have a similar effect (Bogaards et al., 19901 in that increased hepatic concentrations of glutathione and increased activities of glutathione-S-transferase (GSH-S-TI were observed. Indolic compounds produced by the hydrolysis of indolylglucosinolates also induce hepatic monooxygenases and seem to inhibit carcinogenesis (Bradfield and Bjeldanes, 1987). Allyl isothiocyanate, a glucosinolate hydrolysis product, depletes glutathione in vitro (Kawakishi and Kaneko, 1985). Also, glutathione and other thiol compounds promote nitrile compound formation during glucosinolate hydrolysis (Uda et al., 1986). Experiments were conducted, therefore, to determine effects of feeding canola meal on the hepatic glutathione detoxification system and to determine whether canola meal toxicity is modified by supplemental cysteine.


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Department of Nutritional Sciences, University of Guelph, Guelph, Ontario N1G 2W1, Canada



Materials and Methods

Table 2 . Glucosinolate content of canola meals ~

Table 1. Composition of control diet

Ingredient Casein (vitaminfree)' Corn oil" Cornstarchb Mineral mixtureC Vitamin mixtured Cellulosee L-glutamic acide L-methioninee

Amount, g/kg of diet 163 60 678

35 10 42

10 2

q e k l a d Test Diets, Madison, WI. bSt. Lawrence Starch, Pork Credit, Ontario, Canada. CContributed the following per kilogram of diet: CaPH04.2H20, 25.1 g; NaCI, 1.7 g; (MgCO3I4 Mg(OHl2.5HZO, 2.2 g; KzSO,, 5.5 g; C ~ ( C Z H ~ O ~ ) ~ .33.3 H~O mg; ) , KI, .3 mg; FeC13.eHZ0, 333.3 mg; MnCO,, 168.7 mg; Na$3e03, .2 mg; ZnC03, 33.3 mg. dContributed the following per kilogram of diet: choline chloride, 333.3 mg;niacin, 20.0 mg; calcium pantothenate, 20.0 mg; riboflavin, 6.0 mg; thiamin hydrochloride, 6.0 mg; pyridoxine hydrochloride, 6.3 mg; biotin, .2 mg; inositol, 100.0 mg; menadione sodium bisulfite, 60.0 pg; vitamin BI2, 10.0 pg; retinyl palmitate, 4,267 IU; cholecalciferol, 1,113 IU; DL-alpha-tocopherol, 50 IU. Wnited States Biochemical, Cleveland, OH.



Manitoba meal

Alberta meal



2-hydroxy.3.butenyl 2-hydroxy-4-pentenyl 3-butenyl 4-hydroxy.3-indolylmethyl 4-pentenyl 3-indol ylmethyl Total

N D ~ 7.45

.74 ND

1.65 10.38 1.42


6.45 ND



'Values are means of three samples. Units are micromoles per gram. bBelow the limits of detection.

again maintained isoenergetic and isonitrogenous. Traits measured were the same as for the first experiment. In the third experiment, rats were fed either the control diet, the diet containing 400 g of Alberta meal/kg or 400 g of Alberta meal/kg + 6.5 g of cysteine/kg. Rats were fed the control diet for 2 d and then fasted for 3 h before the test diets were fed. All animals were killed a t 1200; 15 rats (five fed each diet) were killed 6 h, 12 h, 1 d, 2 d, 4 d, and 7 d after the commencement of feeding. Rats killed 6 h and 12 h after dosing were fed beginning a t 0600 and 0000,respectively. All others were fed beginning at 1200. CanoZa Meals. The canola meals used were supplied by the Canola Council of Canada, Winnipeg, Manitoba. They were produced from seeds grown on the Canadian prairies during the 1986 crop year and originated from crushing plants in Alberta and Manitoba. According to the prairie grain variety survey for 1986 as provided by the Canola Council of Canada, the meal produced in Alberta would have been mainly from Tobin seed LBrussica carnpestrisl, whereas that from Manitoba would have been mainly from Westar seed (Brassica napus).The meals were analyzed for glucosinolates by the method of Truscott et al. (1983) and the composition is given in Table 2. Statistical Analyses. In the first and second experiments, treatment effects were analyzed by analysis of variance (Snedecor and Cochran, 19671. Student's t-test (Steel and Torrie, 1960) was used in the third experiment to compare animals fed the various treatments with those fed the control diet.

Results Experiment 1. The effects of feeding canola meal on rat BW, feed consumption, BW gain/feed consumed, liver size, hepatic glutathione concentration, and hepatic GSH-S-T activity are given in Table 3. Weight gain was decreased with increasing dietary levels of canola meal (P < .OOll, although there was no difference between the two

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Experimental Design. Male weanling Wistar rats (Charles River Canada Ltd., St. Constant, PQ, initial BW 50 gl were caged in individual stainless steel cages with food and water available a d libitum. The control diet used in all experiments was a casein-based, semipurified diet formulated to meet all nutrient requirements of growing rats (Table 11. In the first experiment, the control diet was modified by addition of two types of canola meal, each added a t 0, 100, 200, 300, and 400 g/kg in an imbalanced factorial design. Additions were made at the expense of casein, and all diets were made isonitrogenous and isoenergetic by varying concentrations of glutamic acid and corn oil. The nine diets were fed for 14 d (10 rats per diet) and feed consumption and BW were monitored. Afterwards, all animals were killed by instantaneous decapitation and livers were excised, weighed, and immediately frozen in liquid nitrogen and stored a t -80°C until they were homogenized and analyzed for glutathione concentration (Tietze, 1969) and GSH-S-T (E.C. activity [Lowry et al., 1951; Bauman et al., 1988). In a second experiment, a total of nine diets were fed (10 rats per diet) with, in addition to the control diet, each of the two types of canola meal supplied a t 400 g/kg and crystalline cysteine. HCl added a t 1.7, 3.2, 4.9, and 6.5 g/kg in a n unbalanced factorial design. Cysteine was added at the expense of glutamic acid, and all diets were



Experiment 3. The effect of duration of feeding of canola meal on hepatic glutathione concentration and hepatic GSH-S-Tactivity is shown in Table 5. There was no indication a t any early time interval that feeding canola meal decreased hepatic glutathione concentrations ( P > .05). In contrast, after 4 d rats fed unsupplemented canola meal had elevated hepatic glutathione concentration (P c .051. Cysteine supplementation enhanced hepatic glutathione concentration at the earlier time intervals (6 and 24 h) and prevented the elevation of glutathione after 4 d of feeding of canola meal. The activities of hepatic GSH-S-T were increased by feeding canola meal after 48 h (P < .051, and supplementation with cysteine prevented this elevation.

Discussion The feeding of either Manitoba (400 g/kg) or Alberta ( > 200 g/kg) canola meals proved toxic to rats, as indicated by reduced growth rate. The relative toxicities of the two meals paralleled the total glucosinolate content of the meals. Alberta meal was more toxic and also contained more than twice as much glucosinolate as Manitoba meal (Table 2). Although indolyglucosinolates have been implicated as being important in the toxicity of canola meal (Bell, 19841, this is not supported by the current study, in which the indolylglucosinolate contents of the meals were similar. Glutathione is a highly reactive nucleophile that protects cells against free radicals and toxic compounds through conjugation reactions cata-

Table 3. Effect of dietary canola meal on growth and hepatic glutathione metabolism in the rat (Exp. 11"

Diet Control Manitoba canola mealc 100 g/kg 200 g/kg 300 g/kg 400 g/kg Mean Alberta canola mealC 100 g/kg 200 g/kg 300 g/kg 400 g/kg Mean Pooled SD

BW gain, g/14 d

Feed consumed, g/14 d

BW gain/ feed consumed

Fresh liver wt, % BW

Hepatic glutathione, Pol/g

Hepatic g1utathione-Stransferaseb







94 89 85 66 84

248 248 257 23 1 246

.372 .35 1 .332 .287 .336

5.50 5.45 5.77 5.29 5.50

9.89 9.97 10.59 9.96 10.10

.578 .769 .769 .790 .727

90 69 56 28 61 11

244 213 203 162 206*** 28

.358 .316 .266 .135 .27 1 ,079

5.53 5.02 5.46 5.30 5.52 .42

10.37 11.56 12.83 12.68 11.86*** 1.20

BO7 .798 .825 .798 .807** .134

&Values are means for IO animals per group. bNanomoles of l-chlorol,4-dinitrobenzeneconjugated per minute per milligram of protein. CFeedingincreasing amounts of canola meal significantly decreased weight gain (P < .001), feed intake (P e .0011, and growth/ feed consumed (P < .05) and increased liver weight (P e .001), hepatic glutathione concentrations (P < .001), and hepatic glutathioneS-transferase activity (P < ,001). **,***Significantlydifferent from mean for rats fed Manitoba canola meal (P < .01 and P e ,001,respectively).

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types of meal ( P > ,051.Feed intake, however, was reduced by increasing levels of canola ( P e .OOl), and this effect was greater for the rats fed Alberta meal than for those fed Manitoba meal. The ratio of BW gain to feed consumed also declined with increasing levels of canola (P c .05). Feeding canola meal increased liver weight when expressed as a fraction of BW (P < .OOl), and the effect was slightly greater for rats fed Alberta meal than for those fed Manitoba meal. Hepatic glutathione concentrations increased with increasing levels of dietary canola meal (P c .0011; this effect was most obvious in the rats fed Alberta meal (P c ,001). Feeding increasing amounts of canola meal also increased hepatic GSH-S-T activity ( P < .001), and the effect again was greater in the animals fed Alberta meal (P < .01). Experiment 2. The effects of supplementing diets containing canola meal with cysteine on growth, feed intake, BW gain/feed consumed, hepatic glutathione concentration, and hepatic GSH-S-T activity are given in Table 4. Rats fed Alberta meal grew more slowly than those fed Manitoba meal, and both groups grew more slowly ( P < .01) and ate less food (P< .001) than controls, regardless of cysteine supplementation. Cysteine supplementation also did not prevent hepatic enlargement when canola meal was fed ( P > .05). Hepatic glutathione concentrations were elevated in all rats fed canola meal (P < . O O l l , regardless of cysteine supplementation. The increased activity of GSH-S-T when canola meal was fed was not seen, however, when cysteine was supplemented (P > ,051.



Table 4. Effect of dietary canola meal and supplemental cysteine on growth and hepatic glutathione metabolism in the rat (Exp.2)"

Diet Control

BW gain, g/14 d 98

Feed consumed, g/14 d 215

BW gain/ feed consumed

Fresh liver wt, oh BW

Hepatic glutathione, Pmol/g

Hepatic glutathione-Stransferaseb





5.15 5.40 5.16 5.24 5.24

14.82 15.83 15.59 15.18 15.36

.lo3 ,196 ,184 ,205 .195

5.48 5.34 5.26 5.83 5.48*** .52

19.48 18.00 18.79 19.68 19.21*** 2.03

.278 .21 1 ,191 ,204 .221 ,073

Manitoba canola meal (400 g/kgIC

3.2 g/kg 4.9 g/kg 6.5 g/kg


77 81 74 76 77

199 203 193 199 199

,386 .399 .381 ,381 ,387

Alberta canola meal (400 g/kgF Supplemental cysteine 1.7 g/kg 3.2 g/kg 4.9 g/kg 6.5 g/kg Mean Pooled SD

40 32 28 44 36" 18

137 125 122 152 134*** 30

.359 ,225 ,181 .249 .254 .153


*Values are means for 10 animals per group. bNanomoles of l-chloro-2,4-dinitrobenzene conjugated per minute per milligram of protein. CFeeding canola meal significantly decreased weight gain (P < ,011and feed intake (P e .0001)and increased liver weight (P e .0011 and hepatic glutathione concentrations (P e .001). **.***Significantly different from mean for rats fed Manitoba canola meal (P < .01 and P < ,001,respectively).

meals, as indicated by the elevated concentrations lyzed by GSH-S-T (Meister, 19881. The hepatic glutathione detoxification system modulates toxicof glutathione and the increased activities of GSHS-T. This response is in contrast to the response of ity of many xenobiotic compounds. Glutathione synthesis is regulated by availability of cysteine. rats to the challenge of toxicants such as Adequate dietary protein is necessary for optimal acetaminophen, which deplete hepatic glutathione reserves (Williamson et al., 1982). It is possible, glutathione synthesis (Bauman et al., 19881, and this effect is largely due to the sulfur amino acid however, that glucosinolates present in the canola meal caused changes through different mechacontent (Chung et al., 1990). Swine fed canola meal nisms affecting the hepatic glutathione detoxificagrew more quickly when diets were supplemented with methionine, but not when they were supple tion system. This hypothesis is supported by the mented with lysine (Bell, 1975). study of Bogaards et al. (19901, in which similar effects were observed when purified glucosinolate It was hypothesized that glucosinolate in the meal may increase the demand for glutathione for hydrolysis products were administered to rats. It is detoxification pathways. Cysteine and cysteine not clear why so many chemically unrelated precursors such as L-2-oxothiazolidine-4-carboxy compounds can elevate hepatic glutathione concentrations beyond control levels in a manner late have been shown to protect against xenobiotic contrary to current ideas about the regulation of challenges by increasing hepatic glutathione the synthetic pathway through feedback inhibireserves Williamson et al., 1982). In the present tion. Two possible mechanisms by which xenobiexperiment, cysteine was supplemented up to the otic compounds elevate hepatic glutathione conlevel of the total cysteine content of a high-protein centrations are proposed: 1) the toxicant causes diet used in earlier studies of glutathione metaboinitial depletion of GSH and compensation of the lism (Bauman et al., 1988). Cysteine supplementaearly depletion by over-repletion of glutathione tion, however, did not overcome the toxicity stores and 2) the toxicant causes a general associated with high levels (400 g/kg) of canola hepatotoxicity and impaired transport of GSH to meal, as indicated by decreased growth and peripheral tissues, perhaps due to reduced activity hepatic enlargement. A more protective effect of gamma-glutamyltranspeptidase,and therefore might be seen, however, if lower levels of canola glutathione accumulates in the liver as a result of meal were fed. liver damage. To determine the possible mechaThe hepatic glutathione detoxification system nism by which canola meal caused elevation of was clearly influenced by the feeding of these

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Supplemental cysteine 1.7 g/kg



Table 5. Hepatic glutathione concentrations and glutathione-S-transferase activities in rats at various time intervals after the commencement of feeding canola meal with and without supplemental cysteine (Exp. 3) Interval after the commencement of feeding Diet

6 h

12 h


48 h

24 h

7 d

Glutathione, pnol/g of liver 5.07' 5.32 6.64* 1.16

5.96 6.18 6.77 .96

3.91 3.95 5.68* 1.61

4.93 5.87 5.52

3.78 7.61* 3.45 2.99


3.49 7.04* 5.70* 2.04

Glutathione-Stransferased Control Alberta canola Alberta canola Pooled SD

+ cysteine

,238 ,253 ,294 .054

.241 ,284 ,229

.233 ,210 ,210 ,040

.056 ~~


,237 .360* ,238 .097

,286 .601* .205 ,206

.200 .470* ,259 ,146


&Values are means for five animals per group. b400 g of Alberta canola meal/kg of diet. '400 g of Alberta canola meal/kg of diet + 6.5 g of cysteine/kg of diet dNanomoles of l-chloro-2,4-dinitrobenzene conjugated per minute per milligram of protein. *Significantly different from controls (P < .05).

hepatic glutathione, one needs to examine the glutathione concentrations at earlier time intervals after feeding canola meals. One limitation of the design of Exp. 1 and 2 was that although a 14-d period was required for adequate measurement of growth, changes in hepatic glutathione reserves would likely occur more quickly and the steady state achieved after 14 d may have masked earlier effects. Such responses were noted by Jaeschke and Wendel, who reported elevated hepatic glutathione concentrations in rats fed butylated hydroxyanisole and butylated hydroxytoluene over 14 d (Jaeschke and Wendel, 1986). Measuring at earlier periods, h o w ever, showed hepatic glutathione stores were first reduced below control levels before accumulating beyond levels thought to be regulated by feedback inhibition of synthesis (Meister, 1988). A similar response has been noted after feeding l-cyano2-hydroxy-3-butene, a glucosinolate hydrolysis product formed from progoitrin (Wallig and Jeffrey, 1990). In the current experiment, however, no initial depletion of glutathione was observed. Accumulation of hepatic glutathione was first observed after 4 d of feeding unsupplemented meal. The accumulation was even greater after 14 d of feeding, as seen in the first two experiments. The accumulation of glutathione seen when unsupplemented canola meal was fed, without the initial depletion, may be indicative of a general hepatotoxicity. Such hepatotoxicity is also reflected in the observed liver enlargement (Exp. 1 and 2). The hepatotoxicity seen with the feeding of canola meal may decrease glutathione transport from the liver to peripheral tissues, thereby resulting in reduced GSH-dependent detoxification of

xenobiotic compounds and increased cellular damage in key target organs such as the thyroid gland. The activity of GSH-S-T may increase in response to glutathione accumulation, and this may also serve as a n index of canola meal toxicity. The elevation in hepatic GSH-S-T activity due to feeding canola, however, was much lower when rats were fed supplemental cysteine. Supplemental cysteine may offer alternative detoxification pathways and alter hepatic utilization of glutathione for detoxification by GSH-S-T when canola meal is fed. Reduction of the effect of canola meal feeding on GSH-S-T activity by cysteine supplementation may reflect a protective effect of cysteine. The effect of dietary cysteine on altering the canola meal-induced changes in glutathione metabolism indicates that dietary modulation can potentially alter xenobiotic detoxification. More knowledge of the biochemical mechanism of canola toxicity is required to devise nutritional strategies, including perhaps other sulfur amino acids and analogues, that may complement advances in plant breeding and permit increased inclusion of canola meal in animal diets.

Implications It was found that feeding canola meal altered the important glutathione detoxification system for breakdown of toxic compounds in the rat liver. The effect of canola meal on the glutathione detoxification system was altered by feeding cysteine. With a better understanding of the biochemical mechanism of canola toxicity, nutritional

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Control Alberta canolab Alberta canola + cysteineC Pooled SD


strategies may be developed that would permit increased feeding of canola meal to livestock.

Literature Cited


Bell, J.M. 1975. Nutritional value of low glucosinolate rapeseed meal for swine. Can. J. Anim. Sci. 55:61. Bell, J. M. 1984. Nutrients and toxicants in rapeseed meal: A review. J. Anim. Sci. 58:996. Boards, J.J.P.,B. van Ommen, H. E. Flke, M. I. Willems, and P. J. van Bladeren. 1990. Glutathione S-transferase subunit induction patterns of brussels sprouts, allyl isothiocyanate and goitrin in rat liver and small intestinal mucosa: A new approach for the identification of inducing xenobiotics. Food Chem. Toxic. 28:81. Bradfield, C. A,, and L. F. Bjeldanes. 1987. Structure-activity relationship of dietary indoles: A proposed mechanism of action as modifiers of xenobiotic metabolism. J. Toxicol. Environ. Health 21:311. Chung, T. K., M. A. Funk, and D. H. Baker. 1990. L-P-oxothiazolidine-4-carboxylate as a cysteine precursor Efficacy for growth and hepatic glutathione synthesis in chicks and rats. J. Nutr. 120:158. Jaeschke, H., and A. Wendel. 1986. Manipulation of mouse organ glutathione contents 11: Time and dose-dependent induction of the glutathione conjugation by phenolic antioxidants. Toxicology 39:59. Kawakishi, S., and T. Kaneko. 1985. Interaction of oxidized

glutathione with allyl isothiocyanate. Phytochemistry 24: 715. Lowry, 0. H., N. J. Rosebrough, A. L. Farr, and R. J. Randall. 1951. Protein measurement with the Folin phenol reagent. J. Biol. Chem. 193:265. Meister, A. 1988. Glutathione metabolism and its selective modification. J. Biol. Chem. 203:17205. Snedecor, G. W., and W. G. Cochran. 1967. Statistical Methods (0th Ed.). Iowa State University Press, Ames. Steel, R.G.D., and J. H. Torrie. 1960. Principles and Procedures of Statistics. McGraw-Hill Book Co., New York. Stoewsand, G. S., J. L. Anderson, and D. J. Lisk. 1986. Changes in liver glutathione-S-transferase activities in coturnix quail fed municipal sludge-grown cabbage with reduced levels of glucosinolates. Proc. SOC.Exp. Biol. Med. 182:95. Tietze, F. 1969. Enzymic method for quantitative determination of nanogram amounts of total and oxidized glutathione: Applications to mammalian blood and other tissues. Anal. Biochem. 27:502. Truscott, R.J.W., I. Minchinton, and J. Sang. 1983. The isolation and purification of indole glucosinolates from Brassica species. J. Sci. Food Agric. 34:247. Uda, Y.,T. Kurata, and N. Arakawa. 1986. Effects of thiol compounds on the formation of nitriles from glucosinolates. Agric. Biol. Chem. 50:2741. Wallig, M. A,, and E. H. Jeffrey. 1990. Enhancement of pancreatic and hepatic glutathione levels in rats during cyanohydroxybutene intoxication. Fundam. Appl. Toxicol. 14:144. Whitty, J. P., and L. F. Bjeldanes. 1987. The effects of dietary cabbage on xenobiotic metabolizing enzymes and the binding of aflatoxin B1 to hepatic DNA in rats. Food Chem. Toxic. 25581. Williamson, J. M., B. Boettcher, and A. Meister. 1982. Intracellular cysteine delivery system that protects against toxicity by promoting glutathione synthesis. Proc. Natl. Acad. Sci. USA 79:6246.

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Bauman, P. F., T. K. Smith, and T. M. Bray. 1988. The effect of dietary protein and sulfur amino acids on hepatic glutathione concentration and glutathione-dependent enzyme activities in the rat. Can. J. Physiol. Pharmacol. 66:


Effect of dietary cysteine supplements on canola meal toxicity and altered hepatic glutathione metabolism in the rat.

Experiments were conducted to determine the effects of feeding canola meal (Brassica campestris and Brassica napus) on the rat hepatic glutathione det...
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