GE Free New Zealand in Food & Environment, 22th July  2003
NZFSA study to help establish safety of herbicides.

GE Free NZ in Food and Environment is pleased to see that an extensive study is being undertaken into glyphosate by the consumer forum of the NZ Food Safety Authority and the ESR (Institute of Environmental Science and Research Ltd). At the FSA consumer forum meeting recently the issue of herbicides was discussed in detail and the forum was notified that the herbicide glyphosate was being safety tested in grains and potatoes. ESR has now outlined a proper and detailed testing programme for ascertaining chemical residue levels in these foods.

A UK House of Commons agriculture committee NFU president Stewart Wells said studies link glyphosate-based herbicides to an increase in fusarium, a black fungus. Laboratory feeding studies on rats caused acute liver injury, chronic liver injury progressing to cirrhosis, and sometimes terminating in hepatocellular carcinoma or cholangiocarcinoma cause serious concerns over this link.

A Danish study has also reported that glyphosate (Roundup) has contaminated drinking water up to five times above the acceptable level. This refutes the assumption that glyphosate is bound in soil and questions the safety of glyphosate use as a herbicide.

" At last the Authority is allowing topical issues to be discussed with input from leading scientists and advisors" said Claire Bleakley of GE Free (NZ) " The GE issue is of great concern and GE foods must be kept out of the diet until they have been clinically trialled to assess levels of safety. Many GE foods have increased herbicide residue levels, yet another reason that they should be proven safe before children and other susceptible people eat them".

A proposal for the next FSA meeting will look in detail at the GE issue and foodborne illness.

Claire Bleakley (06) 3089842

Back to Press Release Directory

Poisonous Spray [Roundup] on a Course Towards Drinking Water
SOURCE: Politken, Denmark, by Anders Legarth Schmidt
English translation sent by NGIN, UK 
10 May 03.htm
Histopathology and gene expression changes in rat liver during feeding of fumonisin B1, a carcinogenic mycotoxin produced by Fusarium moniliforme.

Lemmer ER, de la Motte Hall P, Omori N, Omori M, Shephard EG, Gelderblom WC, Cruse JP, Barnard RA, Marasas WF, Kirsch RE, Thorgeirsson SS.

MRC/UCT Liver Research Centre, University of Cape Town, Observatory, Cape, South Africa.

Fumonisin B1 (FB1) is a carcinogenic mycotoxin produced by the fungus Fusarium moniliforme in corn. Feeding of FB1 to rats causes acute liver injury, chronic liver injury progressing to cirrhosis, and sometimes terminates in hepatocellular carcinoma or cholangiocarcinoma. This study describes the histolopathology and changes in gene expression in the rat liver during short-term feeding of FB1. 

Male Fischer rats were fed either FB1 250 mg/kg or control diet, and were killed weekly for 5 weeks. FB1 caused a predominantly zone 3 'toxic' liver injury, with hepatocyte death due to necrosis and apoptosis. Hepatocyte injury and death were mirrored by hepatic stellate cell proliferation and marked fibrosis, with progressive disturbance of architecture and formation of regenerative nodules.

Despite ongoing hepatocyte mitotic activity, oval cell proliferation was noted from week 2, glutathione S-transferase pi-positive hepatic foci and nodules developed and, at later time points, oval cells were noted inside some of the 'atypical' nodules. Northern blot (mRNA) analysis of liver specimens from weeks 3 to 5 showed a progressive increase in gene expression for alpha-fetoprotein, hepatocyte growth factor, transforming growth factor alpha (TGF-alpha) and especially TGF-beta1 and c-myc. Immunostaining with LC(1-30) antibody demonstrated a progressive increase in expression of mature TGF-beta1 protein by hepatocytes over the 5 week feeding period.

The overexpression of TGF-beta1 may be causally related to the prominent apoptosis and fibrosis seen with FB1-induced liver injury. Increased expression of c-myc may be involved in the cancer promoting effects of FB1.

PMID: 10334199 [PubMed - indexed for MEDLINE]

Back to Press Release Directory