Concentrations of Dieldrin in the Blood and Brain of the Green Sunfish, Lepomis cyanellus, at Death

1971 ◽  
Vol 28 (4) ◽  
pp. 610-612 ◽  
Author(s):  
Roger L. Hogan ◽  
Eugene W. Roelofs

When green sunfish, Lepomis cyanellus, were exposed to concentrations of dieldrin averaging 6 ppb for periods ranging from 124 to 139 hr, the concentrations of dieldrin in the blood and brain at death were approximately 6.0 and 9.0 μg/g. Surviving fish had concentrations markedly lower than those that died. A correlation coefficient of 0.95 was found between concentrations of dieldrin in the blood and in the brain, water dieldrin concentrations having a slight influence on the concentrations in the blood at death. Surviving fish exhibiting severe poisoning symptoms had higher concentrations of dieldrin in the blood and brain than did those showing moderate to minimal symptoms.

1973 ◽  
Vol 30 (7) ◽  
pp. 905-912 ◽  
Author(s):  
Calvin M. Kaya

Previous investigations have demonstrated that stimulation of gonadal recrudescence in the green sunfish (Lepomis cyanellus) depends on the concurrent presence of long photoperiods (15 hr) and elevated temperatures (> 15 C). The present investigation indicates that recrudescence can be stimulated in seasonally regressed ovaries and testes by injections of a crude extract of fish pituitary glands, and in testes by testosterone propionate, but only under elevated temperature. The low temperatures that block gonadal responses to long photoperiods also effectively prevent gonadal responses to administered hormones. These observations indicate that the responsiveness of the gonads of this species to stimulating hormones is markedly modified by temperature; however, the results do not obviate the possibility that secretion of gonadotropins by the brain–pituitary system may also be affected.


1980 ◽  
Vol 84 (1) ◽  
pp. 149-160
Author(s):  
D. H. Bauer ◽  
L. S. Demski

A pattern of dark vertical bands is a characteristic agonistic display in the green sunfish, Lepomis cyanellus and the bluegill, L. macrochirus. The rapidity with which the display can appear and disappear indicates that it is neurally controlled. Electrical stimulation of the brain was carried out in anaesthetized green sunfish and bluegills to map those regions from which this colour change can be elicited. Banding was evoked by stimulation of sites near the midline in the preoptic area, ventral thalamic-dorsal hypothalmic transition zone, the midbrain tegmentum (just dorsal to the nucleus prerotundus pars medialis), in and near the torus semicricularis, in the basal midbrain (region of the crossing tectobulbar tracts), and in the rostral basomedial medulla. A ‘transition’ zone was located basally in the middle medulla, caudal to which only paling was evoked. Areas found to be negative for evoked banding included the telencephalic lobe, the inferior lobe of the hypothalamus, the optic tract, the optic tectum, the body and valvula of the cerebellum and the caudal medulla. It is postulated that the vertical banding pattern is made up of a separate, selectively controlled system of dermal melanophores. The possible neural mechanisms controlling banding are discussed.


Author(s):  
Elsie M. B. Sorensen

The detoxification capacity of the liver is well documented for a variety of substances including ethanol, organic pesticides, drugs, and metals. The piscean liver, although less enzymatically active than the mammalian counterpart (1), contains endoplasmic reticulum with an impressive repertoire of oxidizing, reducing, and conjugating abilities (2). Histopathologic changes are kncwn to occur in fish hepatocytes following in vivo exposure to arsenic (3); however, ultrastructural changes have not been reported. This study involved the morphometric analysis of intracellular changes in fish parynchymal hepatocytes and correlation with arsenic concentration in the liver.Green sunfish (Lepomis cyanellus, R.) were exposed to 0, 30, or 60 ppm arsenic (as sodium arsenate) at 20°C for 1, 2, or 3 week intervals before removal of livers for quantification of the arsenic burden (using neutron activation analysis) and morphometric analysis of ultrastructural alterations. Livers were cut into 1 mm cubes for fixation, dehydration, and embedding.


Author(s):  
E. M. B. Sorensen ◽  
R. R. Mitchell ◽  
L. L. Graham

Endemic freshwater teleosts were collected from a portion of the Navosota River drainage system which had been inadvertently contaminated with arsenic wastes from a firm manufacturing arsenical pesticides and herbicides. At the time of collection these fish were exposed to a concentration of 13.6 ppm arsenic in the water; levels ranged from 1.0 to 20.0 ppm during the four-month period prior. Scale annuli counts and prior water analyses indicated that these fish had been exposed for a lifetime. Neutron activation data showed that Lepomis cyanellus (green sunfish) had accumulated from 6.1 to 64.2 ppm arsenic in the liver, which is the major detoxification organ in arsenic poisoning. Examination of livers for ultrastructural changes revealed the presence of electron dense bodies and large numbers of autophagic vacuoles (AV) and necrotic bodies (NB) (1), as previously observed in this same species following laboratory exposures to sodium arsenate (2). In addition, abnormal lysosomes (AL), necrotic areas (NA), proliferated rough endoplasmic reticulum (RER), and fibrous bodies (FB) were observed. In order to assess whether the extent of these cellular changes was related to the concentration of arsenic in the liver, stereological measurements of the volume and surface densities of changes were compared with levels of arsenic in the livers of fish from both Municipal Lake and an area known to contain no detectable level of arsenic.


2020 ◽  
Vol 12 (1) ◽  
pp. 001-008
Author(s):  
Ting Liu ◽  
Xing-Zhi Liao ◽  
Mai-Tao Zhou

Abstract Background Brain edema is one of the major causes of fatality and disability associated with injury and neurosurgical procedures. The goal of this study was to evaluate the effect of ulinastatin (UTI), a protease inhibitor, on astrocytes in a rat model of traumatic brain injury (TBI). Methodology A rat model of TBI was established. Animals were randomly divided into 2 groups – one group was treated with normal saline and the second group was treated with UTI (50,000 U/kg). The brain water content and permeability of the blood–brain barrier were assessed in the two groups along with a sham group (no TBI). Expression of the glial fibrillary acidic protein, endthelin-1 (ET-1), vascular endothelial growth factor (VEGF), and matrix metalloproteinase 9 (MMP-9) were measured by immunohistochemistry and western blot. Effect of UTI on ERK and PI3K/AKT signaling pathways was measured by western blot. Results UTI significantly decreased the brain water content and extravasation of the Evans blue dye. This attenuation was associated with decreased activation of the astrocytes and ET-1. UTI treatment decreased ERK and Akt activation and inhibited the expression of pro-inflammatory VEGF and MMP-9. Conclusion UTI can alleviate brain edema resulting from TBI by inhibiting astrocyte activation and ET-1 production.


Copeia ◽  
1965 ◽  
Vol 1965 (3) ◽  
pp. 265 ◽  
Author(s):  
John R. Hunter ◽  
Arthur D. Hasler

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