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C. A. Goudie

Publications and source records attributed to C. A. Goudie.

8 recordsLinked to original sources

Tissue distribution and elimination of radiolabelled methyltestosterone fed to sexually undifferentiated blue tilapia

Populations of monosex male Oreochromis aureus can result when the synthetic androgen 17α-methyltestosterone (MT) is fed to sexually undifferentiated fish; however, concerns exist over residues of the androgen remaining in fish destined for human consumption. Radioactivity in the carcass and viscera was evaluated in juvenile fish fed steroid-incorporated diet (tritium and carbon-14 labelled MT and 30 μg unlabelled MT/g feed) for 21 days, and depletion was monitored for 21 days after return to an untreated diet. Radioactivity was detected in the carcass within 1 h after initial feeding and reached highest levels by 6 h. Most of the radioactivity (> 90%) was in the viscera during the 21 days the radio-labelled diet was being fed. Radioactivity was eliminated exponentially, decreasing by 90% within 24 h after the last feeding. After 21 days of feeding untreated diet, < 1% of the original radioactivity remained (representing about 5 ng MT/g of tissue), and was evenly distributed between carcass and viscera. The observed low levels of residual radioactivity at conclusion of the sex reversal period, as well as anticipated dilution through growth during the culture of fish to marketable size, support the conclusion that no potential health hazard exists for people who eat fish that have been fed MT as juveniles.

Aquaculture

Tissue distribution and elimination of radiolabelled methyltestosterone fed to adult blue tilapia

Radioactivity levels in 10 tissues were monitored for 21 days after adult (1-year-old) blue tilapia, Oreochromis aureus , were fed a single meal of a diet containing 30 μg unlabelled methyltestosterone (MT) per gram of feed and radiolabelled MT ( 3 H-labelled steroid nucleus and 14 C-labelled 17α-methyl group). Radioactivity was highest in all tissues 6–12 h after the feeding; about 90% of the radioactivity was in the digestive tract, liver, gall bladder, and kidney. Radioactivity declined nearly 90% by 4 days and only 0.5% of original radioactivity (67 ng/g of fish) remained after 21 days. Half of the remaining exogenous hormone was in digestive and excretory tissues; concentrations in muscle were less than 1 ng/g of tissue. Ratios of 3 H: 14 C in tissues were similar to those incorporated in the diet and suggested that the 17α-methyl group was not removed during metabolism.

Aquaculture

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&ndash;25 C) were 263.6 &plusmn; 11.3 (SE), 38.8 &plusmn; 1.8, and 4.5 &plusmn; 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 &plusmn; 0.06 mg/liter) than at pH 7 or 9 (1.39 &plusmn; 0.06 and 1.49 &plusmn; 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 &plusmn; 16.4 and 1.79 &plusmn; 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