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L Tryphonas

Publications and source records attributed to L Tryphonas.

At least 37 records · Page 2Linked to original sources
PubMed1985

Nerve cell degeneration and progeny survival following ethylenethiourea treatment during pregnancy in rats.

Ethylenethiourea (ETU)-induced early histologic changes in fetal CNS and their effect on postnatal survival was studied at 0, 15 or 30 mg/kg administered as single oral dose on day 13 of pregnancy. Fetuses, from 4-6 dams killed at post-treatment intervals of 12, 24, 48 and 72 h were fixed and studied for histopathological changes following routine methods. The remaining dams were allowed to litter and their progeny was studied for postnatal survival until 80 days of age. Histologic study revealed the presence of karyorrhexis in the germinal layer of basal lamina of CNS extending from the thoracic spinal cord to the telencephalon twelve hours after treatment with 30 mg of ETU/kg. At 48 h post-treatment, the spinal cord showed obliteration and duplication of the central canal and disorganization of germinal and mantle layers. In the brain, the ventricular lining was focally denuded, neuroepithelial cells were arranged in the form of rosettes and the nerve cell proliferation was disorganized. In the 15 mg of ETU/kg group, cellular necrosis was less severe and consisted of degeneration in a single or a small group of cells widely dispersed in the germinal layer of neuraxis. The initial degenerative changes were observed in a specific nerve cell type, identified as the undifferentiated migrating neuroblast. In the postnatal study, since survival was reduced to 50% at the 30 mg/kg and unaffected at the 15 mg/kg, it was concluded that necrosis of neuroblasts up to a certain degree was compatible with postnatal life until adulthood.

Animals↗
PubMed1984

Morphologic evidence for vaginal toxicity of Delfen contraceptive cream in the rat.

The morphologic effects of Delfen contraceptive cream on the female genital tract were evaluated in young female rats given a single per vaginum application (0.1 g/100 g) of this spermicidal agent. Control rats received intravaginal instillates of 0.1 ml/100 g of physiological saline. Immediately after dosing, the vulvas of one-half of the treated and control females were shut by metallic clips to prevent leakage of the material. The females were killed 24 h post-treatment. The genital tracts of all control females were unremarkable. Treated females, with or without vulvar labial apposition, developed acute cervico-vaginitis of varied intensity, but as many as half of those without labial apposition failed to develop any pathologic changes. It was concluded that Delfen cream is capable of causing genital tract injury in rats similar to that induced by an aqueous solution of the active ingredient, nonoxynol-9, and that the incidence of this effect is enhanced if leakage of the cream is prevented by application of vulvar clips.

Animals↗
PubMed1984

Polychlorinated biphenyl (PCB) toxicity in adult cynomolgus monkeys (M. fascicularis): a pilot study.

Aroclor 1254 and Aroclor 1248, at doses of 11.7 and 4.7 mg/kg body weight (equivalent to 5 and 2 mg/kg/day), were given 3 days per week to groups of cynomolgus monkeys, and caused weight loss, fingernail loss, facial edema, epiphora, and death. Blood and adipose tissue PCB concentrations rose with the length of treatment. Tissue concentrations in blood, adipose tissue, liver and kidneys were highest in monkeys treated with Aroclor 1254, reflecting dose differences. There was considerable variation, both within and between groups, in hematologic responses to PCB treatment. Aroclor 1254-treated monkeys had depressed and weakly responsive erythropoiesis. Aroclor 1248-treated monkeys had active but ineffective or depressed erythropoiesis with severe macrocytic or moderate normocytic anemia. Biochemical determination of blood serum constituents revealed treatment and time-related trends towards hypoalbuminemia and increased alkaline phosphatase, serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, lactic dehydrogenase, cholesterol, triglycerides, total bilirubin and direct bilirubin values. Pathologic lesions common in both Aroclor groups were dilatation of meibomian glands duct; mucinous hyperplasia of the gastric mucosa; atrophy and loss of germinal centers in the splenic and other lymphoid follicles; enlargement, fatty degeneration, and necrosis of hepatocytes; bile duct and gall bladder epithelial cell hypertrophy and hyperplasia; and thyroid aberrations in follicular cell size and number of intracytoplasmic lysosomes. Lesions seen exclusively in an Aroclor 1254-treated monkey were widespread mucinous metaplasia and hyperplasia of the fundic mucosa. The results suggest that in general, cynomolgus monkeys may be more refractory or less susceptible to PCB toxicity than rhesus monkeys and, that Aroclor 1248 may be more toxic than Aroclor 1254.

Adipose Tissue↗
PubMed1983

Isoniazid-induced hepatic steatosis in rabbits: an explanation for susceptibility and its antagonism by pyridoxine hydrochloride.

Steatosis was induced in rabbits by subacute administration of isoniazid (INH, 50 mg/kg po). Concomitant treatment with pyridoxine (vitamin B6, 25 mg/kg po) antagonized both development of the hepatic lesions and the elevation of plasma concentrations of lipids. Rabbit acetylating ability was sixfold that of male Wistar rats, a species susceptible to hepatic cell necrosis, whereas hepatic cytochrome P-450 and NADPH-cytochrome c reductase were significantly lower than that observed in control or phenobarbital-induced rats. Examination of the hepatic hydrolysis of the amide bonds of INH and acetylisoniazid (AcINH) indicated that the isonicotinoyl bond of AcINH was the bond most susceptible to amidase hydrolysis in both species; but rabbits possessed the greater amidase activity: 5- to 20-fold greater than control rats and 2- to 7-fold greater than the phenobarbital-induced rats. Consequently, INH-induced hepatic fatty degeneration in rabbits was attributed to increased hepatic exposure to INH-derived primary amine functional groups, and its antagonism by vitamin B6 was attributed to the deactivation of the primary amine by pyridoxal hydrazone formation.

Animals↗
PubMed1983

Interface between pathology and epidemiology in carcinogenesis.

The bottom line here is how or whether our toxicological studies relate to ourselves, to human neoplasia--but the latter is, in important ways, imperfectly defined by the best that can so far be arranged using morphological and epidemiologic methods. There are at least three basic questions: 1) with what precision can the histopathologist define and diagnose cancer in humans--hence emphasis here upon human cancer models, 2) to what extents can difficulties be resolved using animal models, where some similar difficulties are met, and 3) to what extents can epidemiology resolve these difficulties. Not all these problems can be resolved, and the investigator is left with a residue of questions for which no answers are presently available. Some of these are exemplified or precipitated by inconclusive or mistaken diagnoses. In the future awaits practical help from specific biochemical markers and morphometry, but in the present, vigilance and consultation should limit error to a small fraction of observations. In the meantime, existing methods and data are perfectly adequate for study and action in various clinical problems, eg. transmission of familial polyposis of colon, definition and control of various adverse drug reactions.

Epidemiologic Methods↗
PubMed1983

Sequential histopathologic analysis of alpha-hexachlorocyclohexane-induced hepatic megalocytosis and adenoma formation in the HPB mouse.

A temporal, gross, and histologic analysis of the livers of male HPB black mice maintained on a diet containing 500 ppm alpha-hexachlorocyclohexane (alpha-HCH) was performed at 1, 3, 4, 8, 14, 21, 30, 33, 44, and 50 weeks. Grossly, progressive liver enlargement was first noticed at 3 weeks, hepatic nodules at 21 weeks, and emaciation at 30 weeks. Histopathologic liver alterations included universal hypertrophy of centrolobular hepatocytes first seen at 1 week and the merging of adjacent megalocytic zones at 3 weeks. At 21 weeks, microadenomata and macroadenomata were seen in 2 of 7 mice. At 30 weeks, adenomata occurred in 7 of 8 mice and at 33, 44, and 50 weeks in 6 of 6, 5 of 5, and 5 of 5 mice, respectively. Individual adenomata were composed of large well-packed cells with basophilic and acidophilic pale-staining or lipid-laden cytoplasm forming disorganized cords of variable thickness. Depending on the stage of development, adenomata were classified into 4 subtypes. Subtype I, the earliest form seen, arose within megalocytic areas and was composed of a small number of megalocytic cells exhibiting loss of polarity. Subtype II was smaller than a liver lobule. Subtype III was larger and at times resulted from the merging of adjacent subtype II nodules. Subtype IV included the largest adenomata, most of which resulted from coalescing smaller sized subtypes. Under the conditions of this experiment, neither hepatocellular carcinoma nor metastases in the lungs were detected. It was concluded that if alpha-HCH-induced hepatocellular adenoma is ever to give rise to hepatocellular carcinoma, this transformation must progress very slowly.

Adenoma↗
PubMed1979

Reversal by testosterone of atrophy of accessory genital glands of castrated male sheep. A histologic and morphometric study.

The histologic features of male accessory genital glands of entire sheep (group I), castrated sheep (group II), castrated sheep treated with 40 daily intramuscular injections of 50 milligrams testosterone propionate (group III), and castrated sheep treated with 600 milligrams testosterone propionate 72 hours before death (group IV) were compared. Sheep were castrated at 3 months old and all sheep were killed when 15 months old. Volume fractions of glandular tissue, intralobular fibromuscular tissue and perilobular fibromuscular tissue of the seminal vesicles and Cowper's glands fluctuated significantly (P less than 0.05) during postcastration atrophy and after repeated testosterone treatment. Atrophy in sheep in group II was least in the prostate but greatest in Cowper's glands, seminal vesicles and ampullae of vasa deferentia. Seminal vesicle plexi, whose cytons had a statistically significant (P less than 0.05) degree of shrinkage, also were atrophied. After treatment with testosterone the postcastration atrophy of plexal neurons was almost reversed in sheep in group III. There also was hypertrophy of epithelial cells but the testosterone treatment failed to reduce to normal the fibromuscular volume fraction of the accessory genital glands. Testosterone propionate treatment of sheep in group IV failed to elicit appreciable morphologic changes. These results are compared with our previous findings on the content and uptake of zinc by the accessory genital glands. It is suggested that accumulation of zinc in the accessory genital glands of sheep is not necessarily closely linked to normal histologic appearance.

Animals↗
PubMed1978

Choline deficiency and the reversibility of renal lesions in rats.

A transient choline deficiency was induced in young rats subsequently fed a nutritionally complete purified diet during recovery periods of 0 to 119 days. The purpose was to investigate the pathomorphology of the renal lesions and relate this to observed biochemical changes. Acute renal lesions consisting of tubular epithelial cell necrosis and tubulorrhexis were observed in rats immediately after the insult. Chronic renal lesions consisting of interstitial nephritis and scarring were observed 28 to 119 days after the insult; these lesions were qualitatively similar at all times but showed a healing trend as the recovery period lengthened. Kidney and liver weights, liver fat concentration, and serum urea nitrogen concentration were higher in treated rats than in control rats at 0 days (no recovery period allowed) but treatment effects at all other times were minor. Significant changes occurred in serum phenylalanine and tyrosine concentrations and in the phenylalanine to tyrosine ratios after recovery periods of 0, 42 and 84 days. It was concluded that the proximal convoluted tubule was most seriously affected and that the chronic lesions represent a potential threat to kidney function in a stress situation. Some implications for human nutrition are discussed.

Animals↗
PubMed1977

Toxic effects of chlorinated cake flour in rats.

Four experiments were conducted using weanling Wistar rats to determine whether chlorinated cake flour or its constituents were toxic. Levels of 0.2 and 1.0% chlorine added to unbleached cake flour significantly (p less than 0.01) reduced growth rate by 20.7 and 85.2% and increased liver weight relative to body weight by 16.7 and 25.3%, respectively. Lipids extracted from flour chlorinated at the same levels had similar effects. Rat chow diets containing 0.2 and 0.6% chlorine in the form of chlorinated wheat gluten reduced growth rate and increased liver weight as a percentage of body weight. A rat chow diet containing 0.2% chlorine as chlorinated flour lipids increased absolute liver weight by 40%, kidney by 20%, and heart by 10% compared to pair-fed controls.

Amino Acids↗
PubMed1977

Visceral leishmaniasis in a dog: clinical, hematological and pathological observations.

Visceral leishmaniasis was diagnosed in a dog that had been living with his owners in Spain for two years. Clinical diagnosis was somewhat delayed as the disease is largely unknown to Canada and was manifested by a nonresponsive anemia which was not easily explained on peripheral blood evaluation alone, and concomitant interstitial nephritis. On post mortem examination splenomegaly was the main gross pathological finding. Light microscopic examination of bone marrow aspirates and subsequent electron microscopic examination of splenic and hepatic tissues revealed numerous Leishman-Donovan bodies in cells of the reticuloendothelial system. Parasitized reticuloendothelial cells were seen singly or forming granulomata. These latter did not contain giant cells and were confined mainly to the liver and spleen, being sparse and single in the first but extremely numerous and coalescing in the latter. Accumulation of intrafollicular hyaline material was seen in a small number of splenic follicles. Leishman-Donovan bodies on electron microscopic examination had a trilaminar periplast, a large round nucleus with heavy blocks of marginated chromatin and two nucleoli, a short flagellum and a kinetoplast. Lymph nodes and bone marrow had numerous parasitized macrophages but no granulomata. Leishman-Donovan bodies were not detected in the lungs and kidneys both of which exhibited a chronic intersitital reaction. The comparative hematological profile as well as the importance of bone marrow and electron microscopic examinations of the spleen and liver in diagnosis are discussed. The potential public health hazard of leishmaniasis to North America and particularly to Canada is considered.

Animals↗