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B.A. Simco

Publications and source records attributed to B.A. Simco.

10 recordsLinked to original sources

Environmental regulation and influence of the eyes and pineal gland on the gonadal cycle and spawning in channel catfish (Ictalurus punctatus)

Blinded, pinealectomized, or blinded and pinealectomized female channel catfish ( Ictalurus punctatus ) were placed with normal (unoperated on) control fish in outdoor tanks at constant temperature (21 ± 2 C) or earthen ponds (ambient conditions) in February or August, when they were 21 or 27 mo old. Fish were sampled through the following reproductive season. The gonadosomatic index (GSI) and plasma estrogen concentration changed seasonally in 3-yr-old fish, but the changes were less marked or lacking in 2-yr-olds. The GSI levels of sexually mature (≥3 years old) fish peaked about a month earlier in the tanks than in the ponds; the estrogen peak for fish in the tanks was lower than that for pond fish. All experimental fish (both ages) in ponds delayed ovarian resorption for about 1 mo, compared with normal control fish. Exposure to constant 21 C water allowed earlier gonadal recrudescence. All groups of sexually mature fish that were surgically altered in August spawned during the following spring. Fish with eyes spawned earlier and had higher spawning percentages (control 68%, pinealectomized 75%) than did fish without eyes (blinded 50%, blinded and pinealectomized 56%). Neither the eyes nor the pineal is essential for spring gonadal maturation or for spawning in channel catfish, but one or both may have a role in timing these events. An annual internal oscillator that may be modified by environmental temperature is suggested as the primary control of reproductive cycling in the species. Light information obtained through the pineal, eyes, or both appears to affect the time of gonadal resorption.

Ecological and Evolutionary Physiology

Feminization of channel catfish by oral administration of steroid sex hormones

Oral administration of 17‐β‐estradiol or 17‐α‐ethynyltestosterone to sexually undifferentiated channel catfish Ictaturus punctatus during the first 21 days after yolk‐sac absorption resulted in the production of 100% females. The androgen was effective at doses of 6 to 600 μg/g of feed, but not at 0.6 μg/g.

Transactions of the American Fisheries Society

Effects of environmental pH and calcium on ammonia toxicity in channel catfish

The twenty-four-hour median lethal concentrations (24-hour LC50) of total ammonia nitrogen (TA-N) to channel catfish (Ictalurus punctatus) at pH 7, 8, and 9 (total hardness, 40 mg/liter; temperature, 21–25 C) were 263.6 ± 11.3 (SE), 38.8 ± 1.8, and 4.5 ± 0.2 mg/liter, respectively. The 24-hour LC50 of un-ionized ammonia nitrogen (UIA-N) concentration at pH 8 was significantly higher (1.82 ± 0.06 mg/liter) than at pH 7 or 9 (1.39 ± 0.06 and 1.49 ± 0.12 mg/liter). Enrichment of the water to 440 mg/liter total hardness at pH 7 significantly increased the 24-hour LC50 of TA-N and UIA-N (356.3 ± 16.4 and 1.79 ± 0.07). Fish exposed to 25 mg/liter TA-N for 12 hours at pH 7 and 8 showed no differences from control fish in hematocrit, percent total plasma protein, or plasma and muscle chloride. Plasma sodium showed no difference between control and experimental groups at pH 7; however, a significant decrease occurred in fish exposed to 25 mg/liter TA-N at pH 8. No differences in blood pH were found between the control groups and fish exposed to 100 and 200 mg/liter TA-N at pH 7, and to 10 and 25 mg/liter TA-N at pH 8. Plasma sodium depletion is suggested as a contributing mechanism of ammonia toxicity.

Transactions of the American Fisheries Society

Inhibition of nitrite-induced toxicity in channel catfish by calcium chloride and sodium chloride

Environmental chloride has been shown to inhibit methemoglobin formation in fish, thereby offering a protective effect against nitrite toxicity. Channel catfish (Ictalurus punctatus) were simultaneously exposed to various environmental nitrite and chloride levels (as either CaCl 2 or NaCl) in dechlorinated tap water (40 mg/L total hardness, 47 mg/L alkalinity, 4 mg/L chloride, pH = 6.9-7.1, and temperature 21-24°C). Methemoglobin levels in fish simultaneously exposed to 2.5 mg/L nitrite and up to 30 mg/L chloride as either CaCl 2 or NaCl were similar but significantly lower than in unprotected fish. Exposure to 10 mg/L nitrite and 60 mg/L chloride resulted in methemoglobin levels similar to those of the controls; most unprotected fish died. Fish exposed to 10 mg/L nitrite had significantly lower methemoglobin levels when protected with 15.0 mg/L chloride as CaCl 2 than with NaCl. Fish exposed to nitrite in the presence of 60 mg/L chloride (as either CaCl 2 or NaCl) had similar 24-h LC50 values that were significantly elevated above those obtained in the absence of chloride. Calcium had little effect on tolerance to nitrite toxicity in channel catfish in contrast to its large effect reported in steelhead trout (Salmo gairdneri).

Progressive Fish-Culturist

Chloride inhibition of nitrite-induced methemoglobinemia in channel catfish (Ictalurus punctatus)

Exposure of channel catfish (Ictalurus punctatus) fingerlings for 24?h to 1.0, 2.5, and 5.0?mg/L nitrite (pH?=?7; hardness?=?40?mg/L; temperature?=?22–25 °C) produced methemoglobin levels of 20.7?±?1.9%, 59.8?±?1.9%, and 77.4?±?1.4% (SE), respectively. However, methemoglobin levels were not elevated when fish were simultaneously exposed to 1.0, 2.5, and 5.0?mg/L nitrite and 25, 50, and 100?mg/L sodium chloride, respectively. Acclimation to sodium chloride for 24?h before exposure to nitrite did not enhance the inhibitory action of sodium chloride. Fish exposed to 5?mg/L nitrite for 5?h developed 42.5?±?3.8% methemoglobin. When transferred to water containing 5?mg/L nitrite and 250?mg/L sodium chloride, methemoglobin levels returned to normal within 24?h. Environmental chloride probably inhibits methemoglobin formation by competing with nitrite for entrance into the gills of the fish. An ionic ratio of 16 Cl - to 1 NO 2 - is capable of complete suppression of nitrite-induced methemoglobin formation. Bicarbonate ion present in the test water (1?meq/L) may also have contributed to the inhibitive action of chloride.

Journal of the Fisheries Research Board of Canada