PMID- 11451424
OWN - NLM
STAT- MEDLINE
DCOM- 20010920
LR  - 20191105
IS  - 0166-445X (Print)
IS  - 0166-445X (Linking)
VI  - 54
IP  - 1-2
DP  - 2001 Sep
TI  - Effect of beta-naphthoflavone and dimethylbenz[a]anthracene on apoptosis and 
      HSP70 expression in juvenile channel catfish (Ictalurus punctatus) ovary.
PG  - 39-50
AB  - Complex environmental mixtures such as pulp mill effluents and crude oil have 
      been shown to increase ovarian cell apoptosis and affect heat shock protein (HSP) 
      expression in fish. We hypothesize that polyaromatic hydrocarbons (PAH) mediate 
      these effects. To test this hypothesis, we exposed juvenile channel catfish 
      (Ictalurus punctatus) acutely to the aryl hydrocarbon receptor (AhR) agonists, 
      beta-naphthoflavone (BNF; 75 mg/kg) or the model PAH, dimethylbenz[a]anthracene 
      (DMBA; 50 mg/kg) via intraperitoneal injection. Apoptotic DNA fragmentation and 
      HSP70 expression were determined in ovary and liver. Hepatic cytochrome P450 1A 
      (CYP1A) was significantly induced, confirming that BNF and DMBA had distributed 
      to internal organs and stimulated AhR. At 96 h post-injection, BNF and DMBA 
      significantly increased apoptosis and decreased HSP70 expression in juvenile 
      catfish ovaries. Although primary oocytes underwent the greatest rates of 
      apoptosis compared to early or late vitellogenic follicles in all treatment 
      groups, the cell type undergoing increased rates of apoptosis after BNF or DMBA 
      exposure was not clear using terminal deoxynucleotidyl transferase (TdT)-mediated 
      deoxyUTP nick end labeling (TUNEL). There was a significant negative relationship 
      between expression of HSP70 and apoptosis in juvenile channel catfish ovaries. 
      This differed from liver of these fish which did not exhibit increased apoptosis 
      and instead increased hepatic HSP70 expression at 96 h post-injection. However, 
      DMBA had no effect on apoptosis or HSP70 levels in more reproductively mature 
      juvenile fish that were housed at a lower water temperature. This may be due to a 
      developmental or temperature-dependent component to these responses. We propose 
      that the decrease in ovarian HSP70 expression in response to BNF and DMBA may be 
      causally related to the increase in ovarian cell apoptosis. Further experiments 
      using a full time course, dose-response and methods to confirm that AhR is a 
      direct mediator of these effects are required.
FAU - Weber, L P
AU  - Weber LP
AD  - Department of Zoology, 430 Life Sciences West, Oklahoma State University, 
      Stillwater, OK 74078, USA.
FAU - Janz, D M
AU  - Janz DM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Aquat Toxicol
JT  - Aquatic toxicology (Amsterdam, Netherlands)
JID - 8500246
RN  - 0 (HSP70 Heat-Shock Proteins)
RN  - 0 (Receptors, Aryl Hydrocarbon)
RN  - 57-97-6 (9,10-Dimethyl-1,2-benzanthracene)
RN  - 6051-87-2 (beta-Naphthoflavone)
RN  - EC 1.14.14.1 (Cytochrome P-450 CYP1A1)
SB  - IM
MH  - 9,10-Dimethyl-1,2-benzanthracene/*toxicity
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Cytochrome P-450 CYP1A1/biosynthesis
MH  - Female
MH  - HSP70 Heat-Shock Proteins/*biosynthesis
MH  - Ictaluridae
MH  - In Situ Nick-End Labeling
MH  - Ovary/*drug effects/metabolism/pathology
MH  - Receptors, Aryl Hydrocarbon/*physiology
MH  - beta-Naphthoflavone/*toxicity
EDAT- 2001/07/14 10:00
MHDA- 2001/09/21 10:01
CRDT- 2001/07/14 10:00
PHST- 2001/07/14 10:00 [pubmed]
PHST- 2001/09/21 10:01 [medline]
PHST- 2001/07/14 10:00 [entrez]
AID - S0166-445X(00)00179-X [pii]
AID - 10.1016/s0166-445x(00)00179-x [doi]
PST - ppublish
SO  - Aquat Toxicol. 2001 Sep;54(1-2):39-50. doi: 10.1016/s0166-445x(00)00179-x.