James Spencer Bell

Histopathological, hematological, condition-factor, and organ weight changes associated with selenium accumulation in fish from Belews Lake, North Carolina.

Green sunfish (Lepomis cyanellus) were collected from two study sites in Belews Lake, North Carolina, for assessment of correlations between several biological parameters and bioaccumulation of selenium. The fish had elevated concentrations of selenium in the hepatopancreas (liver) and exhibited histopathological and other manifestations of selenium poisoning. Condition-factors of Belews Lake fish were significantly correlated with selenium concentrations in hepatopancreas and skeletal muscle, indicative of capillary permeability changes and resultant edema, supported by the occurrence of significantly increased hepatopancreas-weight-to-body weight ratios in the fish having the higher tissue selenium levels. Gill lamellae were noticeably swollen and vacuolated. Hematocrits of the selenium-contaminated fish were significantly lower than those of the reference fish. The hepatopancreas exhibited lymphocyte infiltration, vacuolation of parenchymal hepatocytes around the central veins, and increased numbers of Kupffer cells. The mesonephros exhibited focal intra-capillary proliferative glomerulonephritis. Hearts showed swollen, inflammatory cell-filled pericardial spaces, diagnosed as possible uremia-induced pericarditis. Ovaries in fish with the higher liver selenium levels exhibited numerous necrotic and ruptured egg follicles. These conditions were observed in the Belews Lake Site 2 fish, but did not occur in reference green sunfish, nor did they occur consistently in fish from the less-contaminated Belews Lake Site 1.

Selenium accumulation and cytotoxicity in teleosts following chronic, environmental exposure

M a r t i n Lake is a 5000 a c r e r e s e r v o i r l o c a t e d in Rusk mad P a n o l a c o u n t i e s in e a s t Texas . F r o m S e p t e m b e r 1978 to May 1979, t h i s l a k e was r e p o r t e d to r e c e i v e aqueous , s e l e n i u m l a d e n e f f l u e n t f rom s y s t e m s used to c o l l e c t f ly ash, s c r u b b e r s ludge , and b o t t o m ash (R.W. L O W E R RE, p e r s o n a l c o m m u n i c a t i o n ) . The absence of n o t e w o r t h y d e t r i m e n t a l p h y s i c o c h e m i c a l p a r a m e t e r s and p e s t i c i d e c o n t a m i n a t i o n in t h e l a k e w a t e r was c o n f i r m e d . Numerous s t ud i e s show t h a t se l en ium is a c c u m u l a t e d to tox ic or l e t h a l l e v e l s in t e l e o s t s p e c i e s (NIELSEN and NIELSEN 1978, S A K U R A Y A M A 1960, ELLIS et al . 1937~ H A L T E R et al. 19809 C A R D W E L L e t al. 1976, A D A M S 1976) and t h a t h i s t o p a t h o l o g i c a l , h e m a t o l o g i c a l , and o t h e r c h a r a c t e r i s t i c changes can r e s u l t f rom s e l e n i u m exposu re (ELLIS e t ai. 1937, H A L T E R et al. 1980, C A R D W E L L et al. 1976). In a c o n t i n u e d e f f o r t to m o n i t o r s e l en ium burdens in c r i t i c a l t i s sues of M a r t i n L a k e f i shes and to e s t a b l i s h b i o l o g i c a l c o r r e l a t e s to t h e s e bu rdens , t h i s s t u d y was u n d e r t a k e n u t i l i z i n g two m e m b e r s of t h e C e n t r a r c h i d a e f a m i l y c o m m o n to T e x a s l a k e s and r e s e r v o i r s . F i sh of the s a m e s p e c i e s were c o l l e c t e d f rom r e f e r e n c e l a k e s for c o m p a r i s o n .

Hepatocyte changes following selenium accumulation in a freshwater teleost.

This report provides morphological and analytical data for a group of green sunfish collected from an area relatively free of metals and a second group of the same species collected from a lake into which selenium had been discharged. Neutron activation data of livers (and kidneys) collected from these fish show an average of about 11 ppm selenium (fresh weight) for both organs; other metals were not detected in the liver (or kidneys) of these fish. Ultrastructural examination of livers from fish of this group showed focal necrosis, areas of granular cytoplasm, fatty infiltration, increased numbers of Kupffer cells, and disorganized liver architecture—compared with those of controls. The presence of massive levels of selenium in the liver and concomitant hepatocyte changes suggests a causal relationship between these phenomena.

Renal changes in selenium-exposed fish

A group of green sunfish was collected from a selenium-rich lake and compared with a similar group collected from a control lake upstream in the same drainage system in east Texas. Since the level of selenium in kidneys of these fish was relatively high (averaging 11 ppm on a fresh weight basis), histopathological and ultrastructural data were collected. Kidneys from fish from the selenium-rich lake showed proliferative glomerulonephritis and hematuria as well as vacuolation and necrosis of cells of the convoluted tubules.

Histopathological changes in selenium-exposed fish

Redear sunfish (Lepomis microlophus) were collected from Martin Lake in east Texas. For at least 8 months, 1 year earlier, aqueous selenium-laden effluent from man-made sources was released into this 5,000-acre reservoir (unpublished data). Redear sunfish from a reference lake, 8 km upstream, were collected for comparison to Martin Lake fish. The hepatopancreas (i.e., liver and associated, disseminated exocrine pancrease), mesonephros (i.e., kidney), gonads, heart, spleen, stomach, and gill arches were preserved for histopathological examination using optical and/or transmission electron microscopy. Livers from Martin Lake redear sunfish (which had accumulated approximately 20 ppm selenium in the liver) showed central necrosis, reduced quantities of rough endoplasmic reticulum and glycogen particles, and increased numbers of lysosome-like structures. Kidneys showed proliferative glomerulonephritis, and exocrine pancreas showed marked hypertrophy at the optical level. Ultrastructurally, architectural disorganization, reduced rough endoplasmic reticulum, increased cisternal space, and proliferation of smooth endoplasmic reticulum were evident. The stomach, spleen, gill, heart, and gonads showed no abnormalities.

Sleep apnea and Q-T interval prolongation—a particularly lethal combination

We have discovered a 20-day-old infant who possessed anatomic evidence of chronic hypoxemia with right ventricular hypertrophy and who died in hypoxic hypoxemia with a postmortem PO2 of 4 mm. Hg. Subsequently, and ECG was discovered which had been obtained at one day of age and showed Q-T interval prolongation along with T-wave alternation. We believe this case to be one of the first to substantiate the mechanism for SIDS as proposed by Schwartz, 26 with hypoxia acting synergistically with a prolonged Q-T interval causing sudden unexpected death in this infant--providing a link between cardiac and respiratory mechanisms of death.

Asphyxiating laryngeal cyst.

Cysts of the larynx are uncommon lesions that on rare occasions may cause sudden death. We report herein the asphyxial death by an obstructing vocal cord cyst in a woman whose body was found in a setting that aroused suspicions of foul play. Features of this case and the autopsy findings are compared with a literature review of laryngeal cysts.

Autopsy of teleosts from contaminated areas.

A systematic procedure provides one method of assessing xenobiotic-induced abnormalities in fish following environmental exposures. Behavioral, external (or gross), histopathological, and internal organ changes allow determination of the severity of toxicant impact on an endemic population provided a sufficient number of specimens is analyzed. Over the past 15 years, these methods have led to the establishment of causal factors in metal- and metalloid-induced toxicity.