Urinary Excretion Of Thiocyanate Research Articles

INFLUENCE OF DIETARY INORGANIC CYANIDE (KCN) ON PLACENTAL THIOCYANATE TRANSFER, TISSUE RIIODANESE ACTIVITY AND PERFORMANCE OF RATS DURING GESTATION

Thirty two bred rats were allotted to two diets to investigate the influence of non-addition or addition of 1000 ppm KCN to cassava — soybean diets on thiocyanate concentrations, tissue rhodanese activity and performance parameters. KCN caus­ed a non-significant (P>0.05) depres­sion in body weight gain but had no effect on weights of liver, kidney and placenta, nor on number and weight of 19 day old foetus. High (1000 ppm) KCN level caused a significant (P<0.05) increase in urinary thiocyanate excretion of thiocyanate. It however had no marked effect on serum protein bound 'iodine, ammiotic fluid thiocyanitte, rhodanese activity of foetal and material tissues nor on foetal thio­cyanate concentration.

Goitrogenic/antithyroidal potential of moringa leaves (Moringa oleifera) and spinach (Spinacia oleracea) of Indian origin on thyroid status in male albino rats

Moringa leaves and spinach used as vegetables containing cyanogens and polyphenols having suspected antithyroidal activity; however, detailed studies in this aspect found unavailable. Goitrogenic/antithyroid potentiality of those plant foods of Indian origin was evaluated. To explore the goitrogenic/antithyroid effect of those plant foods cyanogenic glucosides, glucosinolates, thiocyanate and polyphenol content were measured. These plant foods were fed with diet regularly to adult male albino rats for 30 and 60 days respectively, followed by evaluation of morphological and functional status of thyroid,as thyroid gland weight, the activity status of thyroid hormone synthesizing enzymes viz. TPO, Na+-K+-ATPase, deiodinase I, thyroid hormone profiles, thyroid histoarchitecture as well as urinary iodine and thiocyanate. In moringa leaves and spinach fed diet, there was a significant increase in urinary excretion of thiocyanate and iodine, enlargement of thyroid gland along with hypertrophy of thyroid follicles and altered in the activities of thyroid hormone synthesizing enzymes with concomitant changes of thyroid hormone profiles. Effects were more severe in moringa leaves treated group than that of spinach. Biochemical analysis moringa leaves and spinach reveal that those are rich sources of goitrogens and their prolonged consumption gradually developed a relative state of biochemical and morphological hypothyroidism.

An assessment of the release of inorganic cyanide from the fragrance materials benzyl cyanide, geranyl nitrile and citronellyl nitrile applied dermally to the rat

Organonitriles are widely used as components of fragrances that are incorporated into consumer products, many of which are for human topical use. Some organontriles are readily broken down metabolically to potentially toxic inorganic cyanide. Studies were therefore undertaken to assess whether this occurs with three representative fragrance nitriles, namely, benzyl cyanide, geranyl nitrile and citronellyl nitrile when applied dermally to the rat. The nitriles (benzyl cyanide, 150 mg/kg; geranyl and citronellyl nitriles, 400 mg/kg) were applied to the shaved backs of rats and maintained under occlusion for 24 h. Urine samples were collected for 0–24 h, 24–48 h and 48–72 h from the time of first application. These samples were analysed for thiocyanate, a biomarker for cyanide formation in vivo, as described previously (Potter, J., Smith, R.L., Api, A.M., 2000. Urinary thiocyanate levels as a biomarker for the Generation of inorganic cyanide from benzyl cyanide in the rat. Food and Chemical Toxicology 39, 141–146). In the case of benzyl cyanide, there was a marked increase in urinary thiocyanate levels attributable to the release of cyanide in vivo. The amount of thiocyanate recovered was equivalent to 37% of the dose for males and 32% for females. For geranyl nitrile there was no significant increase in urinary thiocyanate excretion and there was only a marginal increase in the case of citronellyl nitrile that was equivalent to 0.40% of the applied dose for males and 0.29% for females.

DIETARY DEFICIENCY OF CYSTINE AND METHIONINE IN RATS ALTERS THIOL HOMEOSTASIS REQUIRED FOR CYANIDE DETOXIFICATION

Nutritional status is an important factor in modulating the metabolic fate of xenobiotics. Sulfur amino acid (SAA) deficiency has been proposed as a risk factor for human neurological diseases among protein-poor populations subsisting on the cyanophoric plant cassava. Female Sprague-Dawley rats were used to develop and define a model of SAA deficiency for use in future studies examining cassava-related neurotoxicity. Rats were kept in metabolic cages for 7-21 d and fed a balanced diet (BD) of known composition or a comparable diet selectively deficient in methionine and cystine (SAA-free diet). Animals fed the SAA-free diet failed to thrive, lost body weight, excreted porphyrinic materials, and showed a steep and persistent reduction of urinary inorganic sulfate. In contrast, animals on the BD gained body weight and maintained baseline output of urinary inorganic sulfate. Urinary thiocyanate excretion did not differ between groups, but plasma thiocyanate concentrations reached double that in SAA-deficient rats. Increased plasma thiocyanate suggests mobilization of sulfur amino acids from endogenous sources. Liver glutathione and blood cyanide concentrations were similar in animals on the BD and the SAA-deficient diet. In summary, a diet free of methionine and cystine results in increased retention of inorganic sulfur as thiocyanate and a near absence of inorganic sulfur excretion in urine.

Serum Clara Cell Protein: An Indicator of Bronchial Cell Dysfunction Caused by Tobacco Smoking

Clara cell protein (CC16) is a 16-kDa protein secreted by Clara cells and other nonciliated cells of both the bronchiolar and bronchial epithelium. CC16 is present in high concentrations in the respiratory tract secretions but occurs also in other fluids such as serum. In this study, CC16 has been measured in the sera from 65 female and 69 male current smokers and in a sex- and age-matched control group of 135 neversmokers. Lifetime smoking averaged (geometric mean) 12.7 (range, 0.6 to 61.3) and 17.9 (range. 0.8 to 126) pack-years in female and male smokers, respectively. A significant reduction of Clara cell protein was found in the sera of smokers of both sexes. In neversmokers serum CC16 was independent of sex but significantly increased with age. In current smokers serum CC16 was also negatively correlated with both the current and lifetime cigarette consumption and with the 24-h urinary excretion of thiocyanate. After adjustment for age, a linear dose-response relation was apparent between smoking history and serum CC16, the latter decreasing on average by about 15% for each 10 pack-year smoking history. The present study supports the concept that CC16 in serum is a marker of bronchial dysfunction caused by tobacco smoke. As CC16 appears to be a natural immunosuppressor of the respiratory tract, its decreased production might explain some inflammatory changes associated with smoking.

Pathological changes in growing dogs fed on a balanced cassava (Manihot esculenta Crantz) diet.

Studies were carried out to determine the effects of the toxic principle linamarin, a cyanogenic glucoside, in a diet containing cassava (Manihot esculenta Crantz) in the form of gari fed to growing dogs for 14 weeks. There were three groups of dogs, each comprising six animals. One group was fed on a control diet with rice as the carbohydrate source, the second group was fed on cassava (gari) as the carbohydrate source and which was expected to release 10.8 mg HCN/kg cooked food, the third group was fed on the control diet to which enough NaCN was added at feeding time to release 10.8 mg HCN/kg cooked food in order to monitor the effects of the HCN released from gari. All diets contained 130 g crude protein (N x 6.25)/kg and were supplemented with vitamins and minerals. Each animal was given approximately 100 g diet/kg body weight for the duration of the experiment. The biochemical variables investigated were plasma electrolytes, serum proteins, plasma-free amino acids, plasma enzymes and urine protein, and the histology of some metabolically active tissues, namely liver, kidney, myocardium, testis and adrenal gland, was studied. The gari diet caused an elevated plasma thiocyanate concentration (P < 0.01), elevated 24 h urinary thiocyanate excretion and elevated urinary protein excretion (P < 0.01), lowered serum albumin (P < 0.05), a plasma-free amino acid profile which resembled that found in kwashiorkor, lowered plasma K and Ca (P < 0.05). The rice + cyanide diet caused an elevated plasma thiocyanate (P < 0.01) and a 24 h urinary thiocyanate excretion that was significantly higher (P < 0.01) than that of the dogs fed on gari, but caused a urinary protein excretion that was significantly lower than that of the dogs fed on gari (P < 0.01), lowered serum albumin (P < 0.05), a plasma-free amino acid profile that indicated that the amino acids were not being utilized to the same extent as in the control (rice) group but were accumulating. Neither diet had an effect on plasma gamma-glutamyltransferase (EC 2.3.2.2), alanine aminotransferase (EC 2.6.1.2) or isocitrate dehydrogenase (EC 1.1.1.42) activities, plasma Na, Mg, and P concentrations. The gari diet caused generalized congestion and haemorrhage, periportal vacuolation of the liver, swelling, vacuolation and rupture of the epithelial cells of the proximal convoluted tubules of the kidney, myocardial degeneration and adrenal gland degeneration.(ABSTRACT TRUNCATED AT 400 WORDS)

Effect of glutathione modulation on molecular interaction of [ 14C]-chloroacetonitrile with maternal and fetal DNA in mice

Binding of haloacetonitriles or their reactive metabolites to macromolecules of fetal tissue may be responsible for reproductive toxicity. To investigate the role of glutathione (GSH) in the metabolism and reproductive toxicity of haloacetonitriles, irreversible interaction of chloroacetonitrile (CAN) with maternal uterine and fetal DNA was assessed in a time course study among normal and among glutathione-depleted mice treated with [2- 14C]-CAN. GSH was depleted in maternal and fetal tissues by treating of animals with diethylmaleate (DEM) 1 h before [2 14C]-CAN administration. Maternal urinary excretion of thiocyanate was 5 times higher in glutathione-depleted mice than in controls. At 8 and 24 h following [2- 14C]-CAN administration, total radioactivity uptake in maternal uterine tissue, amniotic fluid, and fetal tissue was higher in glutathione-depleted mice than in control. Also the interaction of CAN or its reactive metabolites with maternal uterine DNA was enhanced following glutathione depletion. At 24 h after treatment, the covalent binding to DNA in fetal tissue was significantly increased in glutathione depleted mice (205% of control). The magnitude of interaction of CAN in fetal DNA was about 4 times higher than that in uterine DNA. The time course study in either maternal uterine or fetal DNA revealed elevated and persistent levels of covalent binding of [ 14C]-CAN to DNA at 72 h after treatment. Enhancement of the molecular interaction of CAN in maternal and fetal DNA following GSH depletion indicates an important role for GSH in CAN metabolism.

High α-linolenic acid flaxseed (Linum usitatissimum):some nutritional properties in humans

Although high alpha-linolenic acid flaxseed (Linum usitatissimum) is one of the richest dietary sources of alpha-linolenic acid and is also a good source of soluble fibre mucilage, it is relatively unstudied in human nutrition. Healthy female volunteers consumed 50 g ground, raw flaxseed/d for 4 weeks which provided 12-13% of energy intake (24-25 g/100 g total fat). Flaxseed raised alpha-linolenic acid and long-chain n-3 fatty acids in both plasma and erythrocyte lipids, as well as raising urinary thiocyanate excretion 2.2-fold. Flaxseed also lowered serum total cholesterol by 9% and low-density-lipoprotein-cholesterol by 18%. Changes in plasma alpha-linolenic acid were equivalent when 12 g alpha-linolenic acid/d was provided as raw flaxseed flour (50 g/d) or flaxseed oil (20 g/d) suggesting high bioavailability of alpha-linolenic acid from ground flaxseed. Test meals containing 50 g carbohydrate from flaxseed or 25 g flaxseed mucilage each significantly decreased postprandial blood glucose responses by 27%. Malondialdehyde levels in muffins containing 15 g flaxseed oil or flour/kg were similar to those in wheat-flour muffins. Cyanogenic glycosides (linamarin, linustatin, neolinustatin) were highest in extracted flaxseed mucilage but were not detected in baked muffins containing 150 g flaxseed/kg. We conclude that up to 50 g high-alpha-linolenic acid flaxseed/d is palatable, safe and may be nutritionally beneficial in humans by raising n-3 fatty acids in plasma and erythrocytes and by decreasing postprandial glucose responses.

Alternative sulphur donors for detoxification of cyanide in the chicken

1. Urinary excretion of thiocyanate by hens after dosage with cyanide was studied over 3 hr periods during which various sulphur sources were infused. 2. With 20 μmoles cyanide, endogenous sulphur supplies appeared to be almost sufficient. 3. With 45 μmotes cyanide, thiocyanate excretion was doubled with 90 μmoles of sulphur donor. Higher doses of mercaptopyruvate were also effective but not rhodanese substrates (thiosulphate or methanethio-sulphonate): they interfered with thiocyanate excretion and may also have suppressed its formation. 4. Mercaptopyruvate and rhodanese substrates also differed in their effects on blood cyanide concentration and on the excretion of isotope from radiolabelled cyanide.

Determination of urine thiocyanate in patients with amyotrophic lateral sclerosis.

It has been reported that amyotrophic lateral sclerosis-Parkinsonism-dementia in Guam might be related to the eating of Cycas seeds, which contain cyanide. Based on this assumption, we determined the urinary thiocyanate excretion level in patients with ALS and compared this with that of other neurological diseases. The assay method was designed to use column chromatography with Amberlite IRA 402. The thiocyanate level was determined using pyridine-barbiturate method. The 24-h thiocyanate level was higher in the ALS patients of the middle stages than in the normal control group (Wilcoxon's test, P less than 0.02). There were no significant differences between the ALS patient groups of the early and terminal stages, Kugelberg-Welander disease group, Duchenne type muscular dystrophy group and control group. From these results, we concluded that ALS patients were contaminated with cyanide or thiocyanate and that, along with rapid muscular atrophy, the thiocyanate excretion levels were high.

The relationship of vehicle to target organ toxicology induced by the naturally occurring nitrile 1-cyano-2-hydroxy-3-butene

The effects of gavage vehicle on the acute toxicity of the naturally occurring nitrile 1-cyano-2-hydroxy-3-butene (CHB) were investigated by oral administration of 200 mg/kg body wt/day CHB to male CDF ( F-344 Crl BR) rats for 2 days. The vehicles studied here were distilled water, 5% aqueous Tween 20, and corn oil. Liver, kidney, and pancreas were examined histologically and the differences in lesion incidence and severity were assessed. The effects of gavage vehicle on nitrile-induced elevations of daily urinary thiocyanate excretion and tissue glutathione concentrations were also assessed. The pancreatotoxicity of CHB was present regardless of vehicle and consisted of apoptosis of pancreatic acinar cells, infiltration of pancreatic lobules by macrophages, and acinar atrophy and disorganization. CHB in water alone was associated with the least pancreatotoxic effect, whereas the aqueous Tween vehicle was associated with more severe CHB-induced pancreatic lesions. CHB-induced elevations of tissue nonprotein thiol and glutathione concentrations occurred in all treatment groups, but the values were elevated significantly less in the pancreata of CHB/Tween-treated rats than in those of rats given CHB in water or corn oil. By contrast, the greatest elevation in daily urinary thiocyanate excretion occurred in rats given CHB in aqueous Tween, indicating increased biotransformation of CHB to cyanide when Tween 20 was used as a vehicle. These results illustrate the difficulty of identifying suitable vehicles for administration of lipophilic compounds in toxicology studies.

Sodium nitroprusside, a convenient source of dietary cyanide for the study of chronic cyanide toxicity.

1. The suitability of sodium nitroprusside (SNP) as a source of dietary cyanide has been tested with growing chicks and with hens by measuring plasma or urinary thiocyanate; the major detoxication product of cyanide. 2. Growth and food intake were depressed and plasma thiocyanate concentration was increased in chicks in a progressive manner as the dietary concentration of SNP was increased from 0 to 0.5 g/kg. 3. In laying hens, urinary excretion of thiocyanate was increased fivefold by including SNP in the diet at 0.3 g/kg. 4. It is concluded that SNP is a suitable and convenient source of dietary cyanide for the investigation of chronic cyanide toxicity.

Effect of glutathione depletion on the uptake of acrylonitrile vapors and on its irreversible association with tissue macromolecules

Cellular GSH may influence the metabolism of the rodent brain and forestomach carcinogen acrylonitrile (ACN) and its subsequent binding to tissue macromolecules. To investigate the role of GSH in ACN metabolism and binding to macromolecules, we studied the effect of GSH depletion on the irreversible association of radiolabel with tissue macromolecules in male F-344 rats given a 4 mg/kg dose of [2,3- 14C]ACN by inhalation. A combined phorone/buthionine sulfoximine treatment (300 mg/kg and 2 mmol/kg, respectively) was given 30 minutes prior to ACN exposure to deplete GSH. The uptake of ACN vapor by control rats was biphasic and characterized by a rapid phase lasting about 60 min and by a slower phase from 60 min to the end of exposure. The rate of uptake for both phases was linearly related to the intial concentration of ACN in the chamber. GSH depletion caused an increase in the rate of ACN uptake in both phases. It also caused a decrease in total radioactivity recovered in brain, stomach, liver, kidney, and blood and a concomitant decrease in the ACN-derived nondialyzable radioactivity in these organs. In control rats, accumulation of radiolabel was greatest in brain RNA, but no radioactivity was detected in DNA of any organ examined. In GSH-depleted rats, the radiolabel concentration was higher in brain RNA than in the liver or stomach RNA, but was also 50% lower than that observed in brain RNA of control rats. Urinary excretion of thiocyanate (SCN −), a metabolite derived from the epoxide pathway of ACN metabolism, was doubled in GSH-depleted rats. These results suggest that GSH might be involved in the distribution of ACN-derived reactive species and, therefore, might play a role in the binding of ACN-derived species to tissue macromolecules and nucleic acids.

Effect of glutathione depletion on the irreversible association of acrylonitrile with tissue macromolecules after oral administration to rats

Binding of acrylonitrile and its reactive metabolites to tissue macromolecules, especially nucleic acids, may be responsible for its carcinogenicity in rats. Both acrylonitrile and its primary metabolite, 2-cyanoethylene oxide, also react with glutathione. To better understand the role of glutathione in the manifestation of acrylonitrile toxicity, the irreversible binding to tissue macromolecules was assessed in control and glutathione-depleted F-344 rats treated with a 4 mg/kg dose (po) of [2,3- 14C]acrylonitrile. Glutathione was depleted in rat tissues by the administration of a combined intraperitoneal phorone/buthionine sulfoximine treatment (300 mg/kg and 2 mmol/kg, respectively) given 30 min prior to acrylonitrile administration. The amount of total radioactivity recovered from brain, stomach (target organs), liver, kidney, lung, and blood (nontarget organs) was similar between control and glutathione-depleted rats. However, stomach, lung, blood, and livershowed an increase in total radioactivity content after glutathione depletion by phorone/buthionine sulfoximine treatment. Glutathione depletion also caused an increase in acrylonitrile-derived non-dialysable radioactivity (MW > 3500 Da) in liver, lung, kidney, stomach, blood, and brain macromolecules between 6 and 24 hr after the dose. There was no organ-specific accumulation of radiolabel in RNA in control rats. However, an increase in the radiolabel associated with nucleic acids in the target organs but not in the nontarget organs was measured in glutathione-depleted rats. Urinary excretion of thiocyanate, a metabolite derived from the epoxide pathway, was also increased by 300% in glutathione-depleted rats. These results suggest that glutathione might play a role in the extent of 2-cyanoethylene oxide formation and in the distribution of the radiolabel among tissues.

Detoxication of cyanide in the chicken by conversion to thiocyanate, as influenced by the availability of transferable sulphur

1. 1. The urinary excretion of thiocyanate by hens after dosage with cyanide (30 μmol) has been studied in a series of acute experiments involving 6 hr urine collection periods. 2. 2. More than half of the dose could be recovered as thiocyanate when cyanide was given by intravenous infusion and the rate of excretion closely paralleled plasma thiocyanate concentration. Little cyanide was excreted directly. 3. 3. The excretion of thiosulphate fell by an amount that suggested that availability of sulphane sulphur might limit the extent of conversion. However, neither thiosulphate nor sulphur amino acids enhanced thiocyanate excretion when they were infused together with cyanide; indeed, thiocyanate excretion decreased as the level of sulphur compound given was increased. 4. 4. Both nitrite and sulphite depressed thiocyanate excretion also but they differed in their effects on plasma thiocyanate levels and the pattern of urinary excretion. 5. 5. Comparison of excretion from both sides of the kidneys separately emphasised the importance of the first pass of cyanide in its conversion to thiocyanate. 6. 6. The results suggest that although sulphur availability may be limited the in vivo production of sulphite also restricts cyanide detoxication.

In vivo and in vitro release of cyanide from neurotoxic aminonitriles.

Cyanide release from neurotoxic aminonitriles was measured following in vitro incubation with both microsomes and liver slices. Investigation of cyanide released as urinary thiocyanate following ip aminonitrile administration to rats was also measured. The yield of cyanide in the in vivo study, as measured by the mole percent of administered dose, was greatest from dimethylaminonitrile (DMAA), followed by trimethylaminopropionitrile (TMAPN), dimethylaminopropionitrile (DMAPN), 3,3'-iminodipropionitrile (IDPN), dimethylaminobutyronitrile (DMABN), and monomethylaminopropionitrile (MMAPN). Urinary excretion of thiocyanate accounted for 48.9% of the administered DMAA, 11.6% of TMAPN, 8.0% of DMAPN, 6.8% of IDPN, 3.1% of DMABN, and 1.8% of MMAPN. Incubation of aminonitriles and related compounds with microsomes or liver slices from rats yielded measurable quantities of cyanide from all the compounds tested except for DMABN, TMABN, and succiononitrile. Quantitative evaluation of the yield of formaldehyde by demethylation following microsomal incubation was also determined. The signs of acute toxicity in rats after ip administration of KCN were similar only to those in rats administered DMAA.

Haloacetonitrile excretion as thiocyanate and inhibition of dimethylnitrosamine demethylase: a proposed metabolic scheme.

Haloacetonitriles, contaminants present in chlorinated drinking water, were administered orally to rats, and the urinary excretion of thiocyanate was measured as an index of cyanide release. The urinary excretion of thiocyanate accounted for 14.2% of the dose of monochloroacetonitrile; 7.7-12.8% of the dose of bromochloro-, dichloro-, and dibromoacetonitrile; and 2.25% of the dose of trichloroacetonitrile. The haloacetonitriles inhibited rat-liver microsomal dimethylnitrosamine (DMN) demethylase in an in vitro assay system. Dibromo- and bromochloroacetonitrile were the most potent inhibitors of DMN demethylase, with Ki = 3-4 X 10(-5) M; dichloro- and trichloroacetonitrile were the next most potent, with Ki = 2 X 10(-4) M; and monochloroacetonitrile was the least potent inhibitor, with Ki = 9 X 10(-2) M. Trichloroacetonitrile, but not dibromoacetonitrile, when administered orally inhibited hepatic DMN demethylase activity. The relative capacity of the haloacetonitriles to inhibit DMN demethylase and to be excreted as thiocyanate did not correlate.

Congenital malformations induced by infusion of sodium cyanide in the golden hamster

The teratogenic potential of sodium cyanide was evaluated in the golden hamster. Cyanide was administered continuously by slow infusion to pregnant hamsters of known gestational age. Infusion was by means of subcutaneously implanted osmotic minipumps between Days 6 and 9 of gestation. Infusion of sodium cyanide at dose rates of 0.126, 0.1275, and 0.1295 mmol/kg/hr produced high incidences of malformations and resorptions in the offspring. The most common anomalies seen were neural tube defects, including exencephaly and encephalocoele. Other defects occurred less frequently and included hydropericardium and crooked tail. Fetal crown-rump length was significantly smaller in offspring of cyanide-treated dams than in offspring of control animals. A total dose equivalent to 30 to 40 times the acute sc LD50 dose was administered by infusion to these animals before signs of maternal toxicity appeared. Although signs of toxicity (e.g., weight loss, ataxia, dyspnea) were apparent in some animals, the occurrence of malformations in the offspring was not statistically correlated either with weight loss or with poor health of the dams. Contemporaneous infusion of cyanide and sodium thiosulfate, the classic cyanide antagonist, protected both against the toxic and the teratogenic effects of cyanide. In the presence of thiosulfate, malformations were rarely seen in the offspring, and fetal crown-rump length was similar to controls. Urinary excretion of thiocyanate was not significantly increased in animals treated with thiosulfate; however, concentrations of cyanide and thiocyanate in whole blood were higher in animals receiving only cyanide as compared with hamsters given both agents. The mean whole blood cyanide concentration in hamsters infused with 0.126 mmol/kg/hr sodium cyanide was 25 μ m measured 45 hr after infusion began. Malformations produced by cyanide were similar to those produced by a variety of cyanogenic compounds including aliphatic nitriles and amygdalin. The use of osmotic minipumps adds a new dimension to studies of teratogenic effects. We conclude that cyanide is teratogenic over a narrow range of dose rates.

Cyanide, protein and iodine interactions in the performance, metabolism and pathology of pigs

Performance and metabolic and pathological changes were evaluated in 48 growing pigs fed different levels of dietary protein, cyanide and iodine. Protein deficiency reduced urinary iodine excretion and the concentrations in serum of protein, protein bound iodine and thiocyanate. It also reduced liver rhodanese activity and caused a decrease in urinary thiocyanate excretion which was not significant. Dietary cyanide increased urinary thiocyanate and iodine excretion and serum thiocyanate concentration while the basal diet reduced urinary iodine excretion and serum PBI. Pathological studies showed that cyanide treatment had no marked effect on the microanatomy of the tissues examined. Dietary protein deficiency caused histological changes in the thyroid gland and bone which suggested a decline in metabolic activity. Iodine deficiency caused hyperplastic goitre in the experimental animals.

THE FEEDING VALUE OF TOWER RAPESEED FOR EARLY-WEANED PIGS. I. EFFECTS OF METHODS OF PROCESSING AND OF DIETARY LEVELS

Tower rapeseed (Brassica napus L.), either autoclaved (121 °C, 103 kPa, 30 min), dry-heated (130 °C, 1 h) or extruded (85 °C, 30 sec), was fed to early-weaned pigs in wheat-based diets also containing pea protein concentrate. In the first three experiments, 20 or 24% rapeseed (RS) was included in the diets; in the fourth experiment, 10 and 20% levels of RS were fed. Extrusion and dry heating were only partially effective but autoclaving completely inactivated myrosinase, and reduced isothiocyanate content and the availability of lysine. Thyroid histology and function reflected the goitrogenicity associated with residual myrosinase activity in the processed RS. Increasing the dietary levels of autoclaved RS from zero to 20% of the diet had no effect (P &lt; 0.05) on growth, feed intake, efficiency of utilization of dietary energy and protein or on thyroid or liver weights. Digestibility coefficients for dry matter, protein, energy and crude fibre were reduced at the 20% level of RS. However, hyperplasia and hypertrophy of follicular epithelium were found in thyroids of pigs fed 10 and 20% RS. Thyroxine and protein-bound iodine values tended to decrease, and blood cholesterol and thiocyanate values to increase, with increasing levels of dietary RS. Liver and kidney sections were normal. No glucosinolates were detected in the gastrointestinal tract but urinary thiocyanate excretion increased with the level of RS fed.