PMID- 28259584
OWN - NLM
STAT- MEDLINE
DCOM- 20170522
LR  - 20181202
IS  - 1873-6424 (Electronic)
IS  - 0269-7491 (Linking)
VI  - 224
DP  - 2017 May
TI  - Induced pesticide tolerance results from detoxification pathway priming.
PG  - 615-621
LID - S0269-7491(16)30787-4 [pii]
LID - 10.1016/j.envpol.2017.02.046 [doi]
AB  - Few studies in developmental toxicology have focused on whether early life 
      contaminant exposure affects future susceptibility. Investigations in frogs 
      suggested that early life exposure to a pesticide resulted in higher tolerance to 
      a subsequent challenge. This led to the hypothesis that early-life stage 
      exposures can alter phenotypically plastic traits during development, resulting 
      in induced tolerance. Here, we used Gulf killifish (Fundulus grandis) to test the 
      role of detoxification pathway priming in this inducible tolerance. In frogs, the 
      induced tolerance is present five days after the end of the pre-exposure, but 
      absent after a month. We show that a pre-exposure early in life with carbaryl, 
      induces the activity of cytochrome P450 1A (CYP1A) and increases the ability of 
      pre-exposed groups to metabolize carbaryl, likely because of activation of the 
      aryl hydrocarbon receptor (AHR) pathway. Embryos pre-exposed to carbaryl had a 
      350-500% increase in CYP1A activity, threefold greater capacity to metabolize 
      carbaryl and were more tolerant to a lethal challenge five days after the end of 
      pre-exposure. However, ten days later the differences in CYP1A activity, 
      metabolic capacity and tolerance between pre-exposed and control groups were no 
      longer present. Thus, we conclude that the increase in tolerance observed in 
      pre-exposed fish embryos was due to the activation of the AHR and other metabolic 
      pathways, resulting in a prolonged increase in biotransformation capacity. This 
      allowed individuals to more efficiently deal with subsequent chemical challenges 
      for a short period after the initial pre-exposure. However, this induced 
      tolerance was only short-lived due to the recycling of biotransformation enzymes 
      in the cells as part of general cellular protein maintenance. These findings 
      suggest that induced tolerance was likely due to induction of defense mechanisms 
      during the duration of response to the original stressor, rather than a more 
      permanent change in their ability to respond to future challenges.
CI  - Copyright (c) 2017 Elsevier Ltd. All rights reserved.
FAU - Oziolor, Elias M
AU  - Oziolor EM
AD  - Department of Environmental Science, Baylor University, Waco, TX, 76798, USA; 
      Center for Reservoir and Aquatic Systems Research, Institute for Biomedical 
      Studies, Baylor University, Waco, TX, 76798, USA. Electronic address: 
      elias_oziolor@baylor.edu.
FAU - Howard, Willow
AU  - Howard W
AD  - Department of Environmental Science, Baylor University, Waco, TX, 76798, USA.
FAU - Lavado, Ramon
AU  - Lavado R
AD  - Department of Environmental Science, Baylor University, Waco, TX, 76798, USA.
FAU - Matson, Cole W
AU  - Matson CW
AD  - Department of Environmental Science, Baylor University, Waco, TX, 76798, USA; 
      Center for Reservoir and Aquatic Systems Research, Institute for Biomedical 
      Studies, Baylor University, Waco, TX, 76798, USA. Electronic address: 
      cole_matson@baylor.edu.
LA  - eng
PT  - Journal Article
DEP - 20170301
PL  - England
TA  - Environ Pollut
JT  - Environmental pollution (Barking, Essex : 1987)
JID - 8804476
RN  - 0 (Pesticides)
RN  - 0 (Water Pollutants, Chemical)
RN  - R890C8J3N1 (Carbaryl)
SB  - IM
MH  - Animals
MH  - Carbaryl/*toxicity
MH  - Fundulidae/*metabolism
MH  - Life Cycle Stages/*drug effects
MH  - Pesticides/*metabolism
MH  - Texas
MH  - Water Pollutants, Chemical/*metabolism/*toxicity
OTO - NOTNLM
OT  - Aryl hydrocarbon receptor
OT  - CYP1A
OT  - Carbaryl
OT  - Pesticides
OT  - Phenotypic plasticity
EDAT- 2017/03/06 06:00
MHDA- 2017/05/23 06:00
CRDT- 2017/03/06 06:00
PHST- 2016/08/11 00:00 [received]
PHST- 2017/01/23 00:00 [revised]
PHST- 2017/02/19 00:00 [accepted]
PHST- 2017/03/06 06:00 [pubmed]
PHST- 2017/05/23 06:00 [medline]
PHST- 2017/03/06 06:00 [entrez]
AID - S0269-7491(16)30787-4 [pii]
AID - 10.1016/j.envpol.2017.02.046 [doi]
PST - ppublish
SO  - Environ Pollut. 2017 May;224:615-621. doi: 10.1016/j.envpol.2017.02.046. Epub 
      2017 Mar 1.