Proliferation Of Smooth-surfaced Endoplasmic Reticulum Research Articles

Ultrastructure of feeding sites of the cyst nematode Heterodera schachtii Schmidt in roots of susceptible and resistant Raphanus sativus L. var. oleiformis Pers. cultivars

Ultrastructural changes at feeding sites of the cyst nematode Helerodera schachlii were examined in roots of susceptible and resistant cultivars of Raphanus sativus var oleiformis grown in aseptic nutrient agar culture. Apparently identical changes occurred in both cultivars between 1 and 2 days after invasion by the infective second stage juveniles Induced syncytia (nurse cell systems; derived from parenchymatous cells of the vascular cylinder showed ultrastructural features of high metabolic activity such as a pronounced increase in cytoplasmic density, reduction of the central vacuole into numerous small vacuoles, abundance of ribosonrcs, polyribosotnes, mitochondria, dietyosomes and enlargement of nuclei. Other changes within the syncytia were recorded 3 days after nematode invasion. In the susceptible cultivar there was considerable proliferation of smooth-surfaced endoplasmic reticulum, whereas in the resistant cultivar the endoplasmic reticulum was rough-surfaced with flattened cysternae and there was an incrcrease in vacuolization. Syncytia continued to develop in the susceptible cultivar 4–5 days after nematode invasion, hut disintegrated in the resistant with nearly complete protoplast degeneration 2 days later. Feeding tubes formed by Hardening saliva, were secreted through the stylet aperture of the infective nematode juvenilesinto the initial syncytial cells of both cultivar. The possible function of there tubes for food withdrawal is, discussed.

Morphological changes of the kidney and bone of rats in chronic cadmium poisoning

Wistar rats were given drinking water containing 200 ppm CdCl 2 for 4 to 91 weeks and the kidneys and femoral bones were examined morphologically. Histological examination showed degenerative changes in the proximal convoluted tubules. Electron microscopically tubular changes consisted of cell edema, swelling of mitochondria, proliferation of smooth-surfaced endoplasmic reticulum, vacuolar degeneration, and coagulative necrosis. These alterations were observed to progress with increase of urinary excretion of protein and cadmium levels in the kidneys. Spontanous nephropathy was found more frequently in cadmium-exposed rats than in controls. The bones showed no significant change in histological and roentgenological examinations, as well as in assay of bone mineral content.

Ultrastructural alterations in the liver of rats fed photomirex (8-Monohydromirex)

Alterations in the liver of rats fed photomirex or mirex for 28 d have been studied by electron microscopy. A dose of 0.05 or 0.5 ppm photomirex produced selective ultrastructural damage to the mitochondria of hepatocytes. The parenchymal cells had a proliferation of smooth-surfaced endoplasmic reticulum (SER) with a concomitant depletion of glycogen, a reduction of rough-surfaced endoplasmic reticulum (RER) profiles, an abnormal accumulation of lipid droplets, and pleomorphic nuclei at the 5 ppm photomirex level. In the animals receiving 50 ppm photomirex there were degenerating foci in the organ. There was an increase of electron-dense bodies in the hepatocytes from the 5 ppm mirex group but these cells, in the animals receiving 50 ppm mirex, had SER proliferation and glycogen depletion. It is concluded that photomirex causes more severe ultrastructural changes in the livers of rats than mirex.

Further observations on ultrastructural changes in hepatocytes of mice infected withSchistosoma mansoni

The effect of hepatic granulomas initiated by eggs of Schistosoma mansoni on the ultrastructure of hepatocytes of murine hosts was studied. Specimens of infected livers were collected at half week intervals, starting at week 7 postinfection and terminating at week 9 postinfection. Only the hepatocytes adjacent to granulomas showed any alteration in structure. The most obvious change was the proliferation of smooth-surfaced endoplasmic reticulum, especially striking in samples collected 8 1/2 and 9 weeks postinfection. The hypothesis was presented that the material secreted by the egg of the organism might be responsible for what appeared to be a morphologic detoxification response by the hepatocytes. Other alterations evident in the hepatocytes were an increase in the lysosomal population, mitochondrial changes and a slight hypertrophy of the Golgi complexes. Previous related studies by other investigators were explored and the findings compared with the results of this study.

CYTOCHEMICAL LOCALIZATION OF GLUCOSE 6-PHOSPHATASE ACTIVITY IN THE LIVER OF GROWING MICE AFTER PHENOBARBITAL TREATMENT

The proliferation of the smooth-surfaced endoplasmic reticulum (SER) and the cytochemical localization of glucose 6-phosphatase (G6Pase) activity after phenobarbital treatment were observed in postnatal mouse livers showing rapid proliferation of SER and in adult livers. Animals received one daily intraperitoneal injection of phenobarbital for 3 or 5 days in a dosage of 35mg per kg of body weight for the first 3 days after birth, 50mg per kg for 3 to 9 days after birth, and 50 or 100mg per kg for the adult.Administration of phenobarbital to growing animals did not change the histochemical distribution of G6Pase activity within the liver lobule in contrast with reduction observed in the centrolobular activity in adult animals after the same dose of phenobarbital. An extensive proliferation of SER was noticed in centrolobular hepatocytes from adult animals treated with 100mg per kg of phenobarbital, while no such proliferation occurred after treatment with 50mg per kg of phenobarbital. However, centrolobular hepatocytes of 5- to 10-day-old animals showed a marked proliferation of SER with 50mg per kg of phenobarbital. These observations suggest that there are some differences in the nature of the phenobarbital-induced proliferation of SER between hepatocytes during the postnatal period and fully differentiated hepatocytes of the adult.

Effect of phenobarbital or pregnenolone-16α-carbonitrile (PCN) pretreatment on acute carbon tetrachloride hepatotoxicity in rats

In rats, CCl 4 hepatotoxicity (reflected by augmented serum glutamic-pyruvic transaminase activity and hepatic triglyceride content) was diminished by pregnenolone-16α-carbonitrile (PCN) and markedly increased by phenobarbital. PCN, like penobarbital, caused smooth-surfaced endoplasmic reticulum proliferation in hepatocytes and enhanced hexobarbital oxidation, ethylmorphine N-demethylation, cytochrome P-450 and NADPH-cytochrome c reductase activity. Contrary to earlier views, it is concluded that the increase in these parameters is not a prerequisite for augmented CCl 4 toxicity. Perhaps the cytochrome P-450 induced by the steroid and barbiturate has different catalytic properties, which are responsible for variations in the response to CCl 4.

Ultrastructural changes induced by pregnenolone-16 alpha-carbonitrile in the hepatocytes of thyro-parathyroidectomized and L-thyroxine-treated rats.

Oral administration of pregnenolone-16α-carbonitrile (PCN) to intact thyro-parathyroidectomized or L-thyroxine- treated rats causes an increase of smooth-surfaced endoplasmic reticulum (SER) in hepatocytes. The steroid carbonitrile reduces zoxazolamine paralysis time, and this effect is not modified by L-thyroxine. Hepatocellular SER proliferation, induced by PCN, does not seem to be affected by the thyroid and parathyroid glands.

Effect of pregnenolone-16α-carbonitrile on the hepatic ultrastructure, glycogen content and ethylmorphine N-demethylase activity in pregnant, fetal, and newborn rats

Pregnenolone-16α-carbonitrile (PCN), a potent steroidal microsomal enzyme inducer, increased liver weight, depleted glycogen content, and markedly enhanced hepatic ethylmorphine N-demethylase activity in nonpregnant as well as in 18- and 21-day pregnant rats. Electron microscopy revealed extensive smooth-surfaced endoplasmic reticulum (SER) proliferation in the liver. Mitochondrial abnormalities were noted when the steroid was administered in the last stage of pregnancy. 14C-PCN or its derivative(s) was transported to the fetal liver. The steroid caused glycogen depletion without any detectable change in weight, ultrastructure, or ethylmorphine N-demethylation in the embryo's liver. PCN treatment of neonates produced SER proliferation and significantly increased hepatic weight and enzyme activity. The steroid affected the hepatic tissue of nonpregnant, pregnant, and newborn rats but, except for its effect on glycogen content, it did not act upon the embryonic liver.

Ultrastructural changes induced in the liver of rats by various steroid compounds.

Electron microscopic studies of the rat hepatocytes reveal that SC-11927 leads to extensive proliferation of the smooth-surfaced endoplasmic reticulum (SER). Treatment with ethylestrenol, oxandrolone or hydroxydione results in a less pronounced increase of the smooth membranes. Progesterone, testosterone, estradiol and the non-steroidal stilbestrol induce only an insignificant increase of the SER. Prednisolone, triamcinolone and DOC do not elicit SER proliferation.

A comparative ultrastructural study on drug-induced proliferation of smooth-surfaced endoplasmic reticulum in hepatocytes.

In rats, administration of phenobarbital, 3-methylcholanthrene, spironolactone, cyproterone acetate or pregnenolone-16a-carbonitrile causes proliferation of the smooth-surfaced endoplasmic reticulum (SER) in hepatocytes, without producing marked changes in other cell organelles. The significance of this SER increase and its relationship to microsomal enzyme induction are discussed.

Spironolactone-induced proliferation of smooth-surfaced endoplasmic reticulum in the liver of rats.

Electron microscopic studies revealed that spironolactone, given orally to rats, causes a marked proliferation of smooth-surfaced endoplasmic reticulum in hepatocytes. The characteristic fine structural alterations in the liver may represent the morphologic equivalent of stimulation or induction of drug metabolizing microsomal enzymes and may explain why spironolactone protects rats against the injurious effects of different compounds.

Biochemical Studies on the Drug Metabolism (V)

The effects of food preservatives on the metabolism of drugs were investigated using female rats. Among five preservatives dehydroacetic acid (DHA) showed some stimulating effect on the metabolism of drugs. The pretreatment of female rats with 200mg/kg of DHA daily for 7 or 10 days shortened the duration of hypnosis by 100mg/kg of hexobarbital. The liver preparation from DHA-treated rat had higher activity of N-demethylation of aminopyrine, hydroxylation of hexobarbital or cyclobarbital, aromatic hydroxylation of aniline, and hydrolysis of parathion than control. DHA increased glycogen content but did not change the amount of crude fat in liver. Electronmicroscopical picture of liver from DHA-treated rat showed a marked proliferation of smooth-surfaced endoplasmic reticulum in the hepatic cell. These observations were discussed in connection with the inductive effect of some drugs on the metabolism of drugs.