Alterations in patterns of excretion and other metabolic functions in developing fish embryos exposed to benzo(a)pyrene

Abstract

Steelhead trout (Salmo gairdneri) embryos were used as a model to study some of the physiological and biochemical changes which occur following exposure to sublethal levels of benzo(a)pyrene B(a)P, a known environmental contaminant. Embryos were exposed to B(a)P on day 1, 15, or 25 post fertilization, corresponding to the pre-blastula, eyed stage and late organogenesis stage of development. These times were chosen to determine whether the age of the embryo at the time of exposure influenced their response to this model compound. The changes which were observed were related to the age of the embryo at the time of exposure but not to the concentration of the B(a)P to which they were exposed. It was found that the longer the embryo developed, the more permeable the eggs became, taking up twice to 10 times as much B(a)P on day 25 as they did on day 1. Embryos exposed later in development were also able to excrete the metabolites of B(a)P through the egg membrane 10 times more rapidly than their counterparts which were exposed early during development. Following hatching, the larvae from those groups exposed later in development contained 2 to 5 times as much B(a)P bound to or dissolved in the tissues than did those exposed on day 1. Hatching time was also modified by the times of exposure, with those exposed on days 15 and 25 hatching later and over a longer period of time than either the untreated or DMSO controls. Although physical abnormalities were rare, there appeared to be a consistent increase in the level of teratogenesis in those groups which were exposed early during development.

Biological (molecular and cellular) markers of toxicity

“…This corresponds with the data presented in Kocan and Landolt (1984) where the time to hatching for steellead trout embryos was also extended when exposed to BaP. These researchers theorized that BaP could interfere with the function of hatching enzyme, thereby altering the hatching dynamics of the treated embryos.…”

“…BaP has been shown to cause various developmental abnormalities in steelhead trout embryos after 24 h pulse exposure (2 and 20 #g/ml in DMSO) at specific developmental stages (Kocan and Landolt, 1984). This study demonstrated that the trout embryos were permeable to BaP, could metabolize the parent compound, and excreted some of the metabolites.…”

“…Others have shown that lesser amounts of BaP could both reduce the hatching success of sand sole (Pseaichthys melanostichus) eggs (0.10 jig/L) and produce developmental abnormalities . Kocan and Landolt (1984) observed an extension of the hatching period of the steelhead trout as a result of BaP exposure (2-20 gig/ml on either day 15 or 25 post 71. fertilization). BaP was found to produce similiar effects in Rainbow trout (Hannah et a1., 1982), …”

Clutch morphology and the timing of exposure impact the susceptibility of aquatic insect eggs to esfenvalerate

“…Insect eggs are considered to be more robust and resilient to toxic insult compared with other life stages, but a number of their attributes suggest that this may not always be the case. Developing eggs readily absorb chemicals from their environment, but they may lack the metabolic capacity and behavioral compensation observed in juveniles [3,4]. In addition, previous research with the eggs of other aquatic organisms indicates that embryonic insecticide exposure may result in long‐term impacts on fitness [1].…”

“…Unlike later life stages, eggs lack compensatory behavioral mechanisms (e.g., avoidance drifting) that might protect them from exposure. Metabolic capacity also fluctuates over the course of embryonic development, decreasing to levels as low as those recorded for newly hatched larvae [4]. Furthermore, the finite energy resources available to developing embryos may prevent them from overcoming toxin‐induced energy depletions [5].…”