Vitamin D2 from light-exposed edible mushrooms is safe, bioavailable and effectively supports bone growth in rats.

UNLABELLED: Widespread poor vitamin D status, a health risk for bone disease, increases the need for new food sources of vitamin D. Light-exposed edible mushrooms synthesize vitamin D(2). Bioavailability, safety, and efficacy of high levels of vitamin D(2) from mushrooms to support bone health was established in chronically fed growing rats. INTRODUCTION: Poor vitamin D status from reduced sun exposure is made worse by limited access to vitamin D-containing foods. Exposing white button mushrooms to ultraviolet B (UVB) light markedly increases their vitamin D(2) content, creating a new food source of vitamin D. We used a growing rat model to determine safety, bioavailability, and efficacy in support of bone growth by vitamin D(2) from UVB-exposed mushrooms. METHODS: We fed 150 weanling female rats one of five diets for 10 weeks, all formulated on AIN-93 G. Control diets contained no mushrooms either with or without vitamin D(3). Other diets contained 2.5% and 5.0% of UVB-exposed or -unexposed mushrooms. Safety of the high levels of vitamin D(2) from mushrooms was assessed by animal growth and by Von Kossa staining for soft tissue calcification. Bioavailability was determined from changes in circulating levels of 25-hydroxyvitamin D [25(OH)D] and parathyroid hormone (PTH). Efficacy in support of bone growth was determined from measures of femur bending properties, size, mineralization, and microarchitecture. RESULTS: Diets containing 2.5% and 5.0% light-exposed mushrooms significantly raised 25(OH)D and suppressed PTH levels compared to control-fed rats or rats fed 5.0% mushroom unexposed to light. Microarchitecture and trabecular mineralization were only modestly higher in the light-treated mushroom-fed rats compared to the controls. Von Kossa staining revealed no soft tissue calcification despite very high plasma 25(OH)D. CONCLUSIONS: Vitamin D(2) from UVB-exposed mushrooms is bioavailable, safe, and functional in supporting bone growth and mineralization in a growing rat model without evidence of toxicity.

The Autosow raised miniature swine as a model for assessing the effects of dietary soy trypsin inhibitor.

Toxicological effects of dietary soy trypsin inhibitor (TI) were assessed in male miniature swine, a model chosen for its similarities to human digestive physiology and anatomy. The TI preparation was extracted from defatted raw soy flour. From 1 through 5 weeks of age, piglets were automatically fed either a TI liquid diet [Autosow TI group (ASTI)] or a control liquid diet [Autosow control group (ASC)]. From 6 to 39 weeks of age, these animals received either swine chow and TI or swine chow and control article. The TI diets were formulated to contain a TI activity of approximately 500 mg TI/100 g dry matter. A sow control (SC) group suckled from birth to 6 weeks of age and then fed as the ASC group with swine chow plus control article from 6 to 39 weeks of age. The SC piglets grew faster than ASC piglets during postnatal weeks 1 and 2; however, the ASC piglets were significantly heavier than the SC piglets (P=0.001) at 6 weeks of age. Compared with the ASC group, TI caused a moderate decrease in feed consumption and a moderate but reversible decrease in growth from 2 to 5 weeks of age, but not thereafter. Some control and TI-fed Autosow-reared piglets had loose stools until 6 weeks of age; the effect was significantly greater in the TI-fed group. Otherwise, all swine were active and had normal appearance and behavior.

Pathological evaluation, clinical chemistry and plasma cholecystokinin in neonatal and young miniature swine fed soy trypsin inhibitor from 1 to 39 weeks of age.

The potential toxicity of dietary soy trypsin inhibitor (TI) was evaluated in neonatal miniature swine. From 1 to 6 weeks of age, two groups of male piglets were artificially reared in an Autosow and automatically fed either TI or control liquid diet. From 6 to 39 weeks of age, these two groups were fed either TI or control chow diet. A third group, sow control (SC), suckled from birth to 6 weeks of age, were also weaned to control chow from 6 to 39 weeks of age. Clinical chemistry and plasma cholecystokinin (CCK) determined at 6, 18, 30 and 39 weeks of age, and serum amylase activity with gross and histopathological analyses of major organs at 6 and 39 weeks of age are reported. TI had no effect on plasma CCK, serum amylase activity, or numerous clinical chemistry values. TI-fed piglets had a larger relative liver weight at 6 weeks of age. Relative pancreas weight decreased with age but was not affected by TI. Gross and histopathological analyses of major organs, except the spleen, were within normal limits. Increased incidence of extramedullary hematopoiesis was noted in the spleen of the TI group at 6 but not at 39 weeks of age. There was no consistent pattern in immunohistochemical foci for secretin, gastrin releasing polypeptide or CCK, and no change in DNA, RNA, mitotic index or nuclear density of pancreatic cells. At 6 weeks of age, TI increased pancreatic protein and amylase activity but not trypsin or chymotrypsin activity. None of the effects suggested that this dose of TI was toxic to either the neonatal or sexually mature miniature male swine.

From farm to table to brain: foodborne pathogen infection and the potential role of the neuro-immune-endocrine system in neurotoxic sequelae.

The American diet is among the safest in the world; however, diseases transmitted by foodborne pathogens (FBPs) still pose a public health hazard. FBPs are the second most frequent cause of all infectious illnesses in the United States. Numerous anecdotal and clinical reports have demonstrated that central nervous system inflammation, infection, and adverse neurological effects occur as complications of foodborne gastroenteritis. Only a few well-controlled clinical or experimental studies, however, have investigated the neuropathogenesis. The full nature and extent of neurological involvement in foodborne illness is therefore unclear. To our knowledge, this review and commentary is the first effort to comprehensively discuss the issue of FBP induced neurotoxicity. We suggest that much of this information supports the role of a theoretical model, the neuro-immune-endocrine system, in organizing and helping to explain the complex pathogenesis of FBP neurotoxicity.

Metabolite levels, redox states, and gluconeogenic enzyme activities in livers of rats fed diets containing 1,3-butanediol.

Fat-free diets containing 1,3-butanediol (BD) were fed to rats. The concentration of metabolites in quick-frozen liver and the activities of kidney and liver gluconeogenic enzymes were examined. The free pyridine and adenine nucleotide ratios were calculated from measured intermediary metabolites. The concentrations of lactate, pyruvate, alpha-oxoglutarate, and glucose were significantly decreased in rats fed BD, while the acetoacetate and beta-hydroxybutyrate concentrations were increased in the BD-fed rats. The ratios of the free cytoplasmic [NAD+]/[NADH] and [NADP+]/[NADPH] were significantly decreased. Phosphoenolpyruvate carboxykinase activity was significantly increased in both kidney and liver of rats fed BD. These changes in metabolite levels and enzyme activities paralleled the effects seen in mild starvation, and were similar to reported changes observed when dietary fat was present.

Comparative toxicity of polychlorinated biphenyl and polybrominated biphenylin the rat thyroid gland: light and electron microscopic alterations after subacute dietary exposure.

The comparative toxicity of polychlorinated biphenyl (PCB) and polybrominated biphenyl (PBB) in thyroid glands was studied in male Holtzman rats. Four-week-old animals were fed at dietary levels of 0, 5, 50, and 500 ppm for 5 weeks and then sacrificed. PCB and PBB produced similar dose-dependent ultrastructural lesions in thyroid follicular cells of rats. The daily administration of 5 ppm of either PCB or PBB resulted in the accumulation of large membrane-limited colloid droplets and electron-dense lysosomal bodies within the cytoplasm of follicular cells. Microvilli were short and abnormally branched, and unique cytoplasmic processes extended from the apical surface of follicular cells into the luminal colloid. Similar but more severe ultrastructural changes were observed in thyroid glands of rats administered 50 and 500 ppm of either PCB or PBB. Many follicular cells were distended with large abnormal lysosomal bodies and colloid droplets. Mitochondria were often vacuolated with disrupted cristae. Microvilli were blunt with abnormal branching or absent from areas of the luminal surface of follicular cells. Processes of apical cytoplasm often extended into the follicular lumen in areas devoid of microvilli. Follicular cells remained responsive after the feeding of either PCB or PBB and underwent moderate compensatory hypertrophy and hyperplasia. Thyroid follicles were smaller than in controls and were lined by more columnar cells that occasionally formed papillary projections into the follicular lumens. PCB and PBB produced similar ultrastructural lesions in thyroid follicular cells which appeared to interfere with the synthesis and secretion of thyroxine.

Comparative toxicity of polychlorinated biphenyl and polybrominated biphenyl in the rat liver: light and electron microscopic alterations after subacute dietary exposure.

The comparative toxicity of polychlorinated biphenyl (PCB) and polybrominated biphenyl (PBB) in livers was studied in male Holtzman rats. Four-week-old animals were fed at dietary levels of 0, 5, 50, or 500 ppm for 5 weeks and then sacrificed. The mean liver-body weight ratios of the 50 and 500 ppm groups were increased. Histopathologic examination of the livers revealed fatty degenerative change associated with both compounds. This change was more marked at 500 than at 50 ppm. Various sized lamellar cytoplasmic inclusions were detected in livers of animals fed 500 ppm of either compound. However, the inclusions were more numerous in the PBB-treated rats. Several animals fed 50 ppm PBB had a few inclusions. In rats that received 500 ppm PBB, hypertrophic degenerative hepatocytes were present around the central veins. On the periphery of this change there were occasionally multinucleated hepatocytes. Electron microscopic examination at a dose level of 5 ppm in both the PCB and PBB groups showed a slight proliferation of smooth endoplasmic reticulum (SER), a moderate increase of lipid droplets and some liposomes, and a marked proliferation of Golgi condensing vesicles containing lipoprotein particles. A decreased number of mitochondria and lysosomes was also observed. At 50 ppm, similar but more marked ultrastructural alterations were seen. In addition, an increased number of branched and cup-shaped profiles of mitochondria and a decreased number of Golgi condensing vesicles containing lipoprotein particles were observed. Concentric membranous cytoplasmic whorls were encountered only in the 50 ppm PBB-treated rats. At 500 ppm the number of mitochondria decreased in both groups. There was also a marked increase in the number of SER and liposomes concomitant with a decreased number of Golgi condensing vesicles containing lipoprotein granules. Membranous whorls were also present in the 500 ppm groups.