Translocation of 2,3,7,8-Tetrachlorodibenzo-p-dioxin from Adult Female Lake Trout (Salvelinus namaycush) to Oocytes: Effects on Early Life Stage Development and Sac Fry Survival

1994 ◽  
Vol 51 (6) ◽  
pp. 1410-1419 ◽  
Author(s):  
Mary K. Walker ◽  
Philip M. Cook ◽  
Allan R. Batterman ◽  
Brian C. Butterworth ◽  
Christine Berini ◽  
...  

There were no signs of overt toxicity in sexually mature female lake trout (Salvelinus namaycush) exposed to either a control or a 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-containing diet for 11 wk prior to spawning. At spawning the maternally derived egg TCDD concentrations were 42 ± 4 and 43 ± 6% of the maternal skeletal muscle TCDD concentration on a lipid and wet weight basis, respectively. Egg TCDD concentrations of 233–387 pg TCDD/g egg (wet weight) resulted in nonviable oocytes, while concentrations of 50–152 pg/g resulted in a dose-related increase in sac fry mortality associated with yolk sac edema, craniofacial alterations, and arrested development, resembling blue-sac disease. The dose–response relationship for sac fry mortality associated with blue-sac disease was essentially identical to that observed when fertilized lake trout eggs were exposed to either waterborne or injected TCDD. The no and lowest observable adverse effect levels for sac fry mortality were 23 and 50 pg/g (maternal egg exposure), 34 and 40 pg/g (waterborne egg exposure), and 44 and 55 pg/g (egg injection). LD50s, based on egg TCDD concentration, were 58 (36–90), 69 (64–75), and 80 (68–91) pg/g (95% fiducial limits) following egg exposure via maternal, waterborne, or injection routes, respectively.

1991 ◽  
Vol 48 (5) ◽  
pp. 875-883 ◽  
Author(s):  
Mary K. Walker ◽  
Jan M. Spitsbergen ◽  
James R. Olson ◽  
Richard E. Peterson

Lake trout (Salvelinus namaycush) eggs containing [3H]TCDD concentrations from 0 to 302 parts per trillion (ppt) were observed through the fry stage for TCDD metabolism, elimination, and toxicity. All radioactive residues extracted from eggs and sac fry were due to TCDD; no metabolites were detected. [3H]TCDD was not eliminated from eggs and sac fry, but was rapidly eliminated from fry (t1/2, 35–37 d). Hatchability was less at egg TCDD concentrations [Formula: see text]; however, the greatest TCDD-related mortality occurred during the sac fry stage. In all TCDD groups (34–302 ppt), sac fry that died developed subcutaneous yolk sac edema prior to death, resembling blue-sac disease. The development of yolk sac edema preceded sac fry mortality, and the severity of edema varied directly with cumulative mortality. Based on TCDD concentrations in the egg resulting from a 48-h exposure, the no observable adverse effect level (NOAEL) for mortality was 34 ppt and the lowest observable adverse effect level (LOAEL) was 55 ppt. The TCDD concentration in eggs that caused 50% mortality above control at swim-up (LD50) was 65 ppt. Lake trout sac fry exposed as eggs are more sensitive to the lethal effects of TCDD than any mammalian, avian, or fish species investigated thus far.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Megan M. Knuth ◽  
Debabrata Mahapatra ◽  
Dereje Jima ◽  
Debin Wan ◽  
Bruce D. Hammock ◽  
...  

Abstract Emerging evidence demonstrates the importance of sufficient vitamin D (1α, 25-dihydroxyvitamin D3) levels during early life stage development with deficiencies associated with long-term effects into adulthood. While vitamin D has traditionally been associated with mineral ion homeostasis, accumulating evidence suggests non-calcemic roles for vitamin D including metabolic homeostasis. In this study, we examined the hypothesis that vitamin D deficiency (VDD) during early life stage development precedes metabolic disruption. Three dietary cohorts of zebrafish were placed on engineered diets including a standard laboratory control diet, a vitamin D null diet, and a vitamin D enriched diet. Zebrafish grown on a vitamin D null diet between 2–12 months post fertilization (mpf) exhibited diminished somatic growth and enhanced central adiposity associated with accumulation and enlargement of visceral and subcutaneous adipose depots indicative of both adipocyte hypertrophy and hyperplasia. VDD zebrafish exhibited elevated hepatic triglycerides, attenuated plasma free fatty acids and attenuated lipoprotein lipase activity consistent with hallmarks of dyslipidemia. VDD induced dysregulation of gene networks associated with growth hormone and insulin signaling, including induction of suppressor of cytokine signaling. These findings indicate that early developmental VDD impacts metabolic health by disrupting the balance between somatic growth and adipose accumulation.


2018 ◽  
Vol 610-611 ◽  
pp. 972-982 ◽  
Author(s):  
Sébastien Cambier ◽  
Marthe Røgeberg ◽  
Anastasia Georgantzopoulou ◽  
Tommaso Serchi ◽  
Camilla Karlsson ◽  
...  

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