Rats

The aim of this study was to investigate whether Roundup® (a glyphosate-based herbicide) leads to neurotoxicity in hippocampus of immature rats following acute (30min) and chronic (pregnancy and lactation) pesticide exposure. Maternal exposure to pesticide was undertaken by treating dams orally with 1% Roundup® (0.38% glyphosate) during pregnancy and lactation (till 15-day-old). Hippocampal slices from 15 day old rats were acutely exposed to Roundup® (0.00005-0.1%) during 30min and experiments were carried out to determine whether glyphosate affects 45Ca2+ influx and cell viability. Moreover, we investigated the pesticide effects on oxidative stress parameters, 14C-α-methyl-amino-isobutyric acid (14C-MeAIB) accumulation, as well as glutamate uptake, release and metabolism. Results showed that acute exposure to Roundup® (30min) increases 45Ca2+ influx by activating NMDA receptors and voltage-dependent Ca2+ channels, leading to oxidative stress and neural cell death.

Assessment of whether pesticide exposure is associated with neurodevelopmental outcomes in children can best be addressed with a systematic review of both the human and animal peer-reviewed literature. This review analyzed epidemiologic studies testing the hypothesis that exposure to pesticides during pregnancy and/or early childhood is associated with neurodevelopmental outcomes in children. Studies that directly queried pesticide exposure (e.g., via questionnaire or interview) or measured pesticide or metabolite levels in biological specimens from study participants (e.g., blood, urine, etc.) or their immediate environment (e.g., personal air monitoring, home dust samples, etc.) were eligible for inclusion. Consistency, strength of association, and dose response were key elements of the framework utilized for evaluating epidemiologic studies. As a whole, the epidemiologic studies did not strongly implicate any particular pesticide as being causally related to adverse neurodevelopmental outcomes in infants and children. A few associations were unique for a health outcome and specific pesticide, and alternative hypotheses could not be ruled out. Our survey of the in vivo peer-reviewed published mammalian literature focused on effects of the specific active ingredient of pesticides on functional neurodevelopmental endpoints (i.e., behavior, neuropharmacology and neuropathology). In most cases, effects were noted at dose levels within the same order of magnitude or higher compared to the point of departure used for chronic risk assessments in the United States. Thus, although the published animal studies may have characterized potential neurodevelopmental outcomes using endpoints not required by guideline studies, the effects were generally observed at or above effect levels measured in repeated-dose toxicology studies submitted to the U.S. Environmental Protection Agency (EPA). Suggestions for improved exposure assessment in epidemiology studies and more effective and tiered approaches in animal testing are discussed.

In the present study, ultrastructural alterations induced by oral administration of imidacloprid over 4 weeks was assessed in rats. Forty eight male sprague dawley rats procured from NIN and divided into four groups. Group 1 given with basal diet, group 2 orally gavaged with 80mg/kg/day imidacloprid, group 3 was treated with vitamin C at the rate of 10 mg/kg b.wt/day and group 4 was treated with both imidacloprid and vitamin C
for 4 weeks. In group 2, Ultra thin sections of kidney has evidenced apoptotic nuclei, pleomorphic mitochondria and liver showed swollen nuclei, disrupted chromatin and rough endoplasmic reticulum. Testes revealed increased perinuclear space, disintegrated chromatin, degeneration of spermatids and brain revealed vacuolar mitochondria and apoptotic nuclei. A mild improvement was observed in group 4. In conclusion, these results suggest that exposure to imidacloprid in rats induced ultrastructural alterations and co-administration of vitamin C brought mild protection.

Dose- and term-dependent differences in the location and nature of brain lesions induced in rats and dogs by 2,5-hexanedione (2,5-HD), misonidazole, clioquinol, and acrylamide are reported. Subchronic neuropathies ("distal axonopathy") were induced by low-dose administration of these neurotoxicants and at high doses, lesions caused by acute or subacute neurotoxicity were found in the central nervous system (CNS). In rats, 2,5-HD induced extracellular edema, nerve cell degeneration, and axonal degeneration in the cerebellar and vestibular nuclei. Similar lesions were observed in misonidazole-treated dogs and clioquinol induced nerve cell degeneration in the hippocampus and malacia in the piriform lobes of these animals. In rats, acrylamide induced degeneration of Purkinje cells. Although the mechanism(s) underlying the differential neurotoxicity of high and low doses of these neurotoxicants remains unclear, we suggest certain biochemical mechanisms, cytotoxic edema and excitotoxicity, as factors in the production of such lesions after high-dose treatment.

The European Food Safety Authority (EFSA) has belatedly discovered that the most common genetic regulatory sequence in commercial GMOs also encodes a significant fragment of a viral gene. The finding – published quietly in a new journal [1] - has serious ramifications for crop biotechnology and its regulation, but possibly even more so for consumers and farmers. There are clear indications that this viral gene (called Gene VI) might not be safe for human consumption, although the authors fall short of stating that. It also may disturb the normal functioning of crops, including their natural pest resistance. The authors, Nancy Podevin from the European Food Safety Authority (EFSA) and Patrick du Jardin at University of Liege in Belgium, discovered that of the 86 different transgenic events (unique insertions of foreign DNA) commercialized to-date in the United States 54 contain portions of Gene VI within them. They all have the regulatory sequence called the CaMV 35S promoter (from the cauliflower mosaic virus CaMV), the most commonly used for driving gene expression in GMOs. The events therefore include some of the most widely grown GM crops all over the world such as Roundup Ready soybeans (40-3-2) and MON810 maize. Also included is the controversial NK603 maize recently reported to cause tumours in rats [2] (see also [3] GM Cancer Warning Can No Longer Be Ignored, SiS 56).

European food safety officials have condemned a controversial study that suggested genetically modified vegetables caused tumors in rats and some advocates are calling upon the publishers of the journal in which it appeared to issue a formal retraction. The paper in question was written by University of Caen researcher Gilles-Eric Seralini and suggested that rodents developed tumors and suffered from multiple organ failure after consuming genetically altered corn produced by St. Louis-based Monsanto, according to Kate Kelland of Reuters. In response to criticisms, Reed Elsevier, publishers of Food and Chemical Toxicology, published a statement on their website claiming that Seralini’s work had been “objectively and anonymously peer reviewed.” Furthermore, they said that the authors had made “a series of revisions” and that only then was “the corrected paper then accepted by the editor,” according to E.B. Solomont of the St. Louis Business Journal.