Ultrastructure of Rodlet Cells: Response to Cadmium Damage in the Kidney of the Spot Leiostomus xanthurus Lacépède

Rodlet cell ultrastructure was studied in normal and cadmium-damaged kidney tissues of the spot Leiostomus xanthurus, an estuarine teleost. Rodlet cells in control fish occurred in all parts of the nephron except the renal corpuscle, were oblong to pear-shaped (about 5x10 µm), and contained up to 30 rodlet bodies, a basally situated nucleus, poorly developed mitochondria, and a filamentous cortex. Desmosomes and tight junctions joined rodlet cells to kidney epithelial cells. After cadmium exposure, rodlet cells showed a range of responses from secretory stimulation to necrosis. Rodlet bodies, which were membrane-bound, club-shaped granules, were secreted by a merocrine process, apparently aided by contraction of the fllamentous cortex. New rodlet bodies were assembled in the Golgi apparatus. Mitochondria hypertrophied and developed well-defined cristae. The ultrastructural organization of the rodlet cells in this study and their responses to stimuli suggest that these are tissue or host cells rather than parasites as proposed by some authors. Further studies, however, are needed to confirm the nature of these cells

A Note on the Fine Structure of Myoskeletal Junctions in Acartia tonsa Dana (Copepoda, Calanoida)

The endoskeleton of the calanoid copepod, Calanus finmarchicus, and its muscle attachments were described by Lowe (1935). She reported that the endoskeleton in C. finmarchicus consists of two tendinous endosternites and chitinous exoskeletal ingrowths to which muscles are attached. Howse (1960) noted attachments of the main muscles of the thorax to the exoskeleton in Acartia tonsa. Bouligand (1962) described the ultrastructure of muscle attachments to cuticle in three species of freshwater copepods of the genus Cyclops. Raymont et al. (1974) described the fine structure of muscle attachments to cuticle in C. finmarchicus. Information of the internal anatomy of marine copepods remains sparse. Therefore, we thought it worthwhile to focus our observations on the attachments of muscle to exoskeletal ingrowths in A. tonsa

A Note on the Fine Structure of Myoskeletal Junctions in Acartia tonsa Dana (Copepoda, Calanoida)

The endoskeleton of the calanoid copepod, Calanus finmarchicus, and its muscle attachments were described by Lowe (1935). She reported that the endoskeleton in C. finmarchicus consists of two tendinous endosternites and chitinous exoskeletal ingrowths to which muscles are attached. Howse (1960) noted attachments of the main muscles of the thorax to the exoskeleton in Acartia tonsa. Bouligand (1962) described the ultrastructure of muscle attachments to cuticle in three species of freshwater copepods of the genus Cyclops. Raymont et al. (1974) described the fine structure of muscle attachments to cuticle in C. finmarchicus. Information of the internal anatomy of marine copepods remains sparse. Therefore, we thought it worthwhile to focus our observations on the attachments of muscle to exoskeletal ingrowths in A. tonsa

Hepatocellular Neoplasm in a Wild-Caught Sheepshead Minnow (Cyprinodon variegatus) from the Northern Gulf of Mexico

The sheepshead minnow, Cyprinodon variegatus, is a widely distributed small fish species that inhabits estuaries and inshore waters from New England to northern South America. This species has been used extensively in aquatic environmental toxicity and carcinogenicity tests (Couch et al., 1981; Courtney and Couch, 1984). Hepatic neoplasms have been induced in the sheepshead minnow by exposure to several known chemical carcinogens including diethylnitrosamine (Couch and Courtney, 1987), methylazoxymethanolacetate (Hawkins etal., 1985), and dimethylbenz(a)anthracene (Hawkins et al., 1991). Because of its widespread distribution, limited home range, and proven sensitivity tocarcinogens, the sheepshead minnow appears to be a good candidate to serve as an in situ monitor of environmental carcinogens and other toxicants in coastal waters, especially those of the Gulf of Mexico and Caribbean Sea. To establish background information on the histopathological lesions in sheepshead minnows taken from the wild, we collected and examined specimens from an offshore site presumed to be free of chemical contamination. The present report concerns a hepatic neoplastic lesion, diagnosed as a hepatocellular adenoma, found in a wild sheepshead minnow. Neoplasms from wild sheepshead minnows or spontaneous neoplasms from laboratory specimens previously have not been reported

Hepatocellular Neoplasm in a Wild-Caught Sheepshead Minnow (Cyprinodon variegatus) from the Northern Gulf of Mexico

The sheepshead minnow, Cyprinodon variegatus, is a widely distributed small fish species that inhabits estuaries and inshore waters from New England to northern South America. This species has been used extensively in aquatic environmental toxicity and carcinogenicity tests (Couch et al., 1981; Courtney and Couch, 1984). Hepatic neoplasms have been induced in the sheepshead minnow by exposure to several known chemical carcinogens including diethylnitrosamine (Couch and Courtney, 1987), methylazoxymethanolacetate (Hawkins etal., 1985), and dimethylbenz(a)anthracene (Hawkins et al., 1991). Because of its widespread distribution, limited home range, and proven sensitivity tocarcinogens, the sheepshead minnow appears to be a good candidate to serve as an in situ monitor of environmental carcinogens and other toxicants in coastal waters, especially those of the Gulf of Mexico and Caribbean Sea. To establish background information on the histopathological lesions in sheepshead minnows taken from the wild, we collected and examined specimens from an offshore site presumed to be free of chemical contamination. The present report concerns a hepatic neoplastic lesion, diagnosed as a hepatocellular adenoma, found in a wild sheepshead minnow. Neoplasms from wild sheepshead minnows or spontaneous neoplasms from laboratory specimens previously have not been reported

Rickettsial and Mollicute Infections in Hepatopancreatic Cells of Cultured Pacific White Shrimp (\u3ci\u3ePenaeus vannamei\u3c/i\u3e)

Infections by multiple species of bacteria occurred in hepatopancreatic epithelial cells of cultured Pacific white shrimp (Penaeus vannamei). Grossly, hepatopancreases of moribund shrimp were pale white. Light microscopically, hepatopancreatic tubules appeared atrophied and were associated with granulomas. Examination by scanning and transmission electron microscopy revealed heavy cytoplasmic infections by three forms of microorganisms: (1) a rickettsia-like bacterium, (2) a helical form of a mollicute-like bacterium, and (3) a filamentous mollicute-like bacterium. The rod-shaped rickettsia (900 nm long by 300 nm wide) appeared to be free in the cytoplasm and had both a plasma membrane and a cell wall. Neither form of mollicute possessed a cell wall. The helical mollicute was blunt at its wide end (about 260 nm in diameter) where it contained electron-lucent bodies. Helical turns along its tapered axis resembled those of a spiroplasma (the only helical form of mycoplasma in the class Mollicutes) or a spirochete. The helical bacterium did not possess periplasmic flagella characteristic of spirochetes, which lends support to its being a type of spiroplasma. The filamentous mollicute consisted of masses of short, branched filaments 60 nm wide with intermittent spherical dilations and terminal blebs on the branches. The presumed mollicutes have not been reported previously in crustaceans. Each bacterium, or concurrent infections of the bacteria, are pathogenic to cultured shrimp, could impact culture operations, and thus deserve more study

Effects of Space Shuttle Exhaust Plumes on Gills of Some Estuarine Fishes: A Light and Electron Microscopic Study

The first few launches of the space shuttle resulted in fish kills in a lagoon near the launch site. To study this phenomenon further, sheepshead minnow (Cyprinodon variegatus), sailfin molly (Poecilia latipinna), and mosquitofish (Gambusia affinis) were exposed to the exhaust plume in buckets placed near the launch site. An open bucket provided a full exposure, a partly closed one provided an intermediate exposure, and a closed one was the control. Three h after launch, the pH of the water from the full exposure had decreased from about 7 to about 3, Al and Fe levels had increased, and some fish had died. Gills ol most fishes from full exposures and some from intermediate exposures were damaged. Gills, however, exhibited no aneurysms, mucus coagulation, or hemorrhaging. Some secondary lamellae swelled, some fused with adjacent lamellae, and others clubbed or retracted into the filament. Many lamellar pavement cells died and sloughed off. Mucous cells of intermediate exposure specimens bulged on the filament surface and pavement cells lost their microridges. Mineral deposits, probably aluminum oxide, occurred on gills of fishes from full exposures. Focally, pavement cells were eroded exposing the underlying structures. The sudden pH drop in the full exposures probably caused the gill damage. However, we could not determine the effect of previous exposure on the experimental fish, or whether gill damage was the lethal lesion. The possibility is indicated that some fish recover after exposure to the exhaust plume

Ultrastructure of Lymphocystis in the Heart of the Silver Perch, Bairdiella chrysura (Lacépède), Including Observations on Normal Heart Structure

The fine structure of normal heart muscle from the silver perch, Bairdiella chrysura (Lacépède), is similar to that previously reported for marine and freshwater teleosts. Cardiac lymphocystis is a viral disease manifested by single, giant-cell lesions variously located in the epicardium, trabecular spaces, and subendocardium – in direct apposition to myocardial cells. Occasionally, the hyaline capsule of lymphocystis cells partially surround myocardial cells but cause no pathological changes or inflammatory reaction. The lymphocystis cells contain typical cellular organelles, including the viroplasmic net unique to these cells. Annulate lamellae, often continuous with the rough endoplasmic reticulum, are present, usually along the periphery of the cell. Some elements of the rough endoplasmic reticulum are dilated and contain a finely granular material, but others contain cross-banded fibrils, each having a periodicity of 30 nm. Similar fibrils are present in the perinuclear cisternae

TMEM97 and PGRMC1 do not mediate sigma-2 ligand-induced cell death

Abstract Sigma-2 receptors have been implicated in both tumor proliferation and neurodegenerative diseases. Recently the sigma-2 receptor was identified as transmembrane protein 97 (TMEM97). Progesterone receptor membrane component 1 (PGRMC1) was also recently reported to form a complex with TMEM97 and the low density lipoprotein (LDL) receptor, and this trimeric complex is responsible for the rapid internalization of LDL. Sigma-2 receptor ligands with various structures have been shown to induce cell death in cancer cells. In the current study, we examined the role of TMEM97 and PGRMC1 in mediating sigma-2 ligand-induced cell death. Cell viability and caspase-3 assays were performed in control, TMEM97 knockout (KO), PGRMC1 KO, and TMEM97/PGRMC1 double KO cell lines treated with several sigma-2 ligands. The data showed that knockout of TMEM97, PGRMC1, or both did not affect the concentrations of sigma-2 ligands that induced 50% of cell death (EC50), suggesting that cytotoxic effects of these compounds are not mediated by TMEM97 or PGRMC1. Sigma-1 receptor ligands, (+)-pentazocine and NE-100, did not block sigma-2 ligand cytotoxicity, suggesting that sigma-1 receptor was not responsible for sigma-2 ligand cytotoxicity. We also examined whether the alternative, residual binding site (RBS) of 1,3-Di-o-tolylguanidine (DTG) could be responsible for sigma-2 ligand cytotoxicity. Our data showed that the binding affinities (K i) of sigma-2 ligands on the DTG RBS did not correlate with the cytotoxicity potency (EC50) of these ligands, suggesting that the DTG RBS was not fully responsible for sigma-2 ligand cytotoxicity. In addition, we showed that knocking out TMEM97, PGRMC1, or both reduced the initial internalization rate of a sigma-2 fluorescent ligand, SW120. However, concentrations of internalized SW120 became identical later in the control and knockout cells. These data suggest that the initial internalization process of sigma-2 ligands does not appear to mediate the cell-killing effect of sigma-2 ligands. In summary, we have provided evidence that sigma-2 receptor/TMEM97 and PGRMC1 do not mediate sigma-2 ligand cytotoxicity. Our work will facilitate elucidating mechanisms of sigma-2 ligand cytotoxicity