Developmental Immunotoxicity of Imidacloprid in Wistar Rats

Human exposure to imidacloprid is likely to occur during its use as an acaricide or an ectoparasiticide. Accordingly, the developmental immunotoxic potential of imidacloprid was investigated. Oral exposure was initiated in timed pregnant female Wistar rats on gestation day 6 (GD 6) till GD 21. On GD 20, half of the gravid dams were sacrificed, and in utero fetal development was assessed. In the other half of the dams, administration was continued till weaning on postnatal day 21 (PND 21) and maternal toxicity was investigated. A subgroup of weaned pups was sacrificed to assess immunotoxicity parameters. The other half of the pups were exposed to imidacloprid till PND 42, and immunotoxicity was assessed. The findings revealed post-implantation loss in the highest dose group, indicating the risk of abortion. Soft tissue abnormalities and skeletal alterations were observed in the highest dose group. Humoral immunity was assessed by estimating hemagglutination titer and immunoglobulin production. Cell mediated immunity was assessed by Delayed Type Hypersensitivity, whereas, non-specific immunity was assessed by phagocytic index, and other phenotypic parameters. These data revealed that imidacloprid caused age-dependent adverse effects on the developing immunity which was aggravated when exposure continued throughout development, leading to a compromised immune system.

EFSA noemt artikel in verband met GGO-maïs en tumoren bij ratten van onvoldoende wetenschappelijke kwaliteit

De Europese Voedselautoriteit (EFSA) stelt dat het recent gepubliceerde artikel met betrekking tot tumoren bij ratten die GGO-maïs en/of glyfosaat gevoederd kregen van onvoldoende wetenschappelijke kwaliteit is om als waardevol beschouwd te worden voor de evaluatie van de risico's. De eerste analyse door EFSA wijst er op dat het concept, het systeem van rapportering van de gegevens en de analyse van de studie, zoals in het artikel beschreven, inadequaat zijn.

Un estudio alerta sobre la toxicidad de los transgénicos y relanza el debate

Un estudio francés que asegura que las ratas alimentadas con maíz transgénico sufren cáncer y mueren antes, apoyado con fotografías de tumores grandes como pelotas de ping-pong, relanzó este miércoles la polémica sobre estos organismos genéticamente modificados. "Por primera vez en el mundo, un transgénico y un pesticida han sido estudiados por su impacto en la salud a más largo plazo de lo que habían hecho hasta ahora las agencias sanitarias, los gobiernos y la industria. Los resultados son alarmantes", aseguró Gilles-Eric Seralini, profesor de la Universidad de Caen y director del estudio.

Mit Genmais gefütterte Ratten sterben viel früher

Französische Forscher haben Ratten über einen längeren Zeitraum mit Genmais gefüttert – mit alarmierenden Ergebnissen: Die Tiere sind vergleichsweise deutlich früher gestorben – die meisten an Krebs. Die Ergebnisse seien "alarmierend", sagte Gilles-Eric Seralini, Professor an der Universität Caen und Experte für gentechnisch veränderte Organismen (GVO) in Nahrungsmitteln.

Frankrijk erg bezorgd over gen-maïs

Frankrijk en de EU onderzoeken met spoed of een genetisch gemodificeerde maïssoort leidt tot kanker. Het gaat om de maïssoort NK603 van fabrikant Monsanto. De soort is ontwikkeld om beter bestand te zijn tegen het onkruidbestrijdingsmiddel Roundup. De maïskorrels worden nu ingevoerd in de EU. Zo nodig zal Frankrijk direct een Europees verbod vragen, meldde premier Jean-Marc Ayrault donderdag. In de studie, onder leiding van Gilles-Eric Séralini van de universiteit van Caen en Criigen, werd het effect van NK603 Roundup Ready-maïs onderzocht. Het Franse onderzoek dat is gepubliceerd in vakblad Food and Chemical Toxicology, duurde 2 jaar, ongeveer de levensduur van de rat.

GM foods cause cancer in chronic rat study and may behave likewise in humans

Rats fed a lifelong diet of one of the bestselling strains of genetically modified corn suffered tumours and multiple organ damage, according to a controversial French study published today. Scientists said the results raised serious questions about the safety of GM foods and the assurances offered by biotech companies and governments. The first lifetime trials involving rats fed on GM corn found a raised incidence of breast tumours, liver and kidney damage. Dr Michael Antoniou, a molecular biologist at King’s College, London, and an expert on GM foods, said: ‘It shows an extraordinary number of tumours developing earlier and more aggressively – particularly in female animals. I am shocked by the extreme negative health impacts.’

The neonicotinoids may adversely affect human health, especially the developing brain

There have been a few studies of neonicotinoid-induced toxicity in the nervous systems of vertebrates, and these studies were conducted with only a few of the neonicotinoids, such as imidacloprid, thiamethoxam, and clothianidin. Imidacloprid has been reported to act as an agonist or an antagonist of nAChRs at 10 microM in rat pheochromocytoma (PC12) cells and to change the membrane properties of neurons at concentrations greater then or equal to 10 microM in the mouse cochlear nucleus. Exposure to imidacloprid in utero causes decreased sensorimotor performance and increased expression of glial fibrillary acidic protein (GFAP) in the motor cortex and hippocampus of neonatal rats. Furthermore, it has been reported that the neonicotinoids thiamethoxam and clothianidin induce dopamine release in the rat striatum via nAChRs and that thiamethoxam alters behavioral and biochemical processes related to the rat cholinergic systems. Recently, imidacloprid and clothianidin have been reported to agonize human alpha4beta2 nAChR subtypes. This study is the first to show that acetamiprid, imidacloprid, and nicotine exert similar excitatory effects on mammalian nAChRs at concentrations greater than 1 microM. In the developing brain, alpha4beta2 and alpha7 subtypes of the nAChR have been implicated in neuronal proliferation, apoptosis, migration, differentiation, synapse formation, and neural-circuit formation. Accordingly, nicotine and neonicotinoids are likely to affect these important processes when it activates nAChRs. Accumulating evidence suggests that chronic exposure to nicotine causes many adverse effects on the normal development of a child. Perinatal exposure to nicotine is a known risk factor for sudden infant death syndrome, low-birth-weight infants, and attention deficit/hyperactivity disorder. Therefore, the neonicotinoids may adversely affect human health, especially the developing brain.

Nicotine exposure together with genes in the dopaminergic system confer risk for ADHD

Attention deficit hyperactivity disorder (ADHD) is a multifactorial disorder and both genetic and environmental factors have been implicated in its etiology. Yet, the interaction between genes and environment is seldom studied directly. This article considers the plausibility of nicotine exposure during prenatal development as well as postnatal factors in the etiology of ADHD. The few existent studies show inconsistent results, but provide preliminary evidence suggesting that nicotine exposure together with genes in the dopaminergic system confer risk for ADHD.

The Dynamic Effects of Nicotine on the Developing Brain

Nicotinic acetylcholine receptors (nAChRs) regulate critical aspects of brain maturation during the prenatal, early postnatal, and adolescent periods. During these developmental windows, nAChRs are often transiently upregulated or change subunit composition in those neural structures that are undergoing major phases of differentiation and synaptogenesis, and are sensitive to environmental stimuli. Nicotine exposure, most often via tobacco smoke, but increasingly via nicotine replacement therapy, has been shown to have unique effects on the developing human brain. Consistent with a dynamic developmental role for acetylcholine, exogenous nicotine produces effects that are unique to the period of exposure and that impact the developing structures regulated by acetylcholine at that time. Here we present a review of the evidence, available from both the clinical literature and preclinical animal models, which suggests that the diverse effects of nicotine exposure are best evaluated in the context of regional and temporal expression patterns of nAChRs during sensitive maturational periods, and disruption of the normal developmental influences of acetylcholine. We present evidence that nicotine interferes with catecholamine and brainstem autonomic nuclei development during the prenatal period of the rodent (equivalent to first and second trimester of the human), alters the neocortex, hippocampus, and cerebellum during the early postnatal period (third trimester of the human), and influences limbic system and late monoamine maturation during adolescence.

Nicotine is a neural teratogen

Preclinical studies, using primarily rodent models, have shown acetylcholine to have a critical role in brain maturation via activation of nicotinic acetylcholine receptors (nAChRs), a structurally diverse family of ligand-gated ion channels. nAChRs are widely expressed in fetal central nervous system, with transient upregulation in numerous brain regions during critical developmental periods. Activation of nAChRs can have varied developmental influences that are dependent on the pharmacologic properties and localization of the receptor. These include regulation of transmitter release, gene expression, neurite outgrowth, cell survival, and synapse formation and maturation. Aberrant exposure of fetal and neonatal brain to nicotine has been shown to have detrimental effects on cholinergic modulation of brain development. These include alterations in sexual differentiation of the brain, and in cell survival and synaptogenesis. Long-term alterations in the functional status and pharmacologic properties of nAChRs may also occur, which result in modifications of specific neural circuitry such as the brainstem cardiorespiratory network and sensory thalamocortical gating. Such alterations in brain structure and function may contribute to clinically characterized deficits that result from maternal smoking, such as sudden infant death syndrome and auditory-cognitive dysfunction. Although not the only constituent of tobacco smoke, there is now abundant evidence that nicotine is a neural teratogen.