Rat kidney cancers determined by dietary ochratoxin A in the first year of life
File(s)
Published version
Author(s)
Mantle, PG
Type
Journal Article
Abstract
An experiment to explore renal carcinogenic efficacy of male rat exposure to dietary
ochratoxin
A (OTA) only in the first year of life has been made in comparison to lifetime
exposure. Ten months exposure to OTA at 300 μg/kg b.w. was sufficient to cause high
incidence of tumours which became apparent clinically after a latency of up to a year. As a
putative model for human kidney cancer, the study shows a silent organ
-
specific
carcinogenic effect through protracted exposure up to middle age and focused probably on
very few nephrons. So far, tumourigenesis has not been
recognised
until in the last qua
rter
of natural rat life, but for OTA, rat renal carcinogenesis requires both long exposure and
only during the first year of normal longevity. The present findings offer an experimental
framework within which systematic histopathology during tumourigenesi
s might show
whether findings of mechanistic studies in key focal neoplasms can reasonably be applied
to OTA as a putative renal carcinogen for idiopathic kidney cancer in humans. Already, the
rat tumours mimic those occurring spontaneously in the Eker rat
, and there is disparity
between the large necessary OTA exposure in the rat and the trace amounts of OTA
consumed by humans. In all such complex considerations it is important to adhere
rigorously to established principles of disease epidemiology.
ochratoxin
A (OTA) only in the first year of life has been made in comparison to lifetime
exposure. Ten months exposure to OTA at 300 μg/kg b.w. was sufficient to cause high
incidence of tumours which became apparent clinically after a latency of up to a year. As a
putative model for human kidney cancer, the study shows a silent organ
-
specific
carcinogenic effect through protracted exposure up to middle age and focused probably on
very few nephrons. So far, tumourigenesis has not been
recognised
until in the last qua
rter
of natural rat life, but for OTA, rat renal carcinogenesis requires both long exposure and
only during the first year of normal longevity. The present findings offer an experimental
framework within which systematic histopathology during tumourigenesi
s might show
whether findings of mechanistic studies in key focal neoplasms can reasonably be applied
to OTA as a putative renal carcinogen for idiopathic kidney cancer in humans. Already, the
rat tumours mimic those occurring spontaneously in the Eker rat
, and there is disparity
between the large necessary OTA exposure in the rat and the trace amounts of OTA
consumed by humans. In all such complex considerations it is important to adhere
rigorously to established principles of disease epidemiology.
Date Issued
2016-09-25
Date Acceptance
2016-08-18
Citation
Journal of Kidney Cancer and Vhl, 2016, 3 (3), pp.1-10
ISSN
2203-5826
Publisher
Codon Publications
Start Page
1
End Page
10
Journal / Book Title
Journal of Kidney Cancer and Vhl
Volume
3
Issue
3
Copyright Statement
© 2016 Peter George Mantle. This work is licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/)
Sponsor
Commission of the European Communities
Grant Number
QLK1-CT-2001-01614
Publication Status
Published
Date Publish Online
2016-09-25