Rats

This study was undertaken to explore relationships between level of imidacloprid in the serum and semen quality among men farmers in addition to investigating histopathological findings in treated mature male rats. Our research entailed two parts; firstly, human part done on farm workers (n=35) with age between (Mean ± SD 34.3±6.4) and healthy volunteers (n=25) their ages were (35.6±8.2) years old asked to provide semen and blood samples.

One year ago, an agency of the World Health Organization’s International Agency for Cancer Research (IARC) declared that glyphosate (or Roundup), the world’s most widely used herbicide, probably causes cancer. Then, in the fall, the European Food Safety Agency’s (EFSA) responded with an assessment that disagreed with the WHO’s findings. In response, 94 scientists came out in support of the IARC’s original findings. This week, the group—which includes scientists from around the world—released their article in the peer-reviewed Journal of Epidemiology and Community Health saying: The most appropriate and scientifically based evaluation of the cancers reported in humans and laboratory animals as well as supportive mechanistic data is that glyphosate is a probable human carcinogen. On the basis of this conclusion and in the absence of evidence to the contrary, it is reasonable to conclude that glyphosate formulations should also be considered likely human carcinogens. And their endorsement is no small matter. In fact, as the U.S. Environmental Protection Agency (EPA) reassesses the safety of glyphosate, and the U.S. Food and Drug Administration (FDA) plans to begin testing food for its residue, this volley has important implications.

Developmental neurotoxicity (DNT) studies are designed to investigate whether pre- or post-natal exposure to a toxicant affects neural development. Bayer conducted such a study with imidacloprid. Imidacloprid was administered in the diet to mated Sprague Dawley rats. The females were treated from gestation day 0 to 20 and then continued through the lactation day 21 at doses of 0, 100, 250 and 750 ppm, corresponding to an average daily intake of 0, 8, 19 and 54.7 mg/kg/day during gestation. The pups were indirectly exposed to imidacloprid for a total of 41 days (20 days in utero and 21 days via lactation). After weaning on postnatal day 21 pups were given untreated feed. Brain tissue from 10 pups/sex/group were analyzed on postnatal days 11 and 75. On post-natal day 11, female pups from the 750 ppm group had a decreased caudate putamen width (-5.5%) and a substantial reduction in the thickness of the corpus callosum (-27.6%). Morphometric brain measurements were not performed in the intermediate and low dose groups. The EFSA Panel on Plant Protection Products and their Residues (PPR) expressed concern about this pattern and although it does not directly demonstrate neurotoxicity, it cannot be dismissed, especially considering the magnitude of decrease in corpus callosum dimension. The major point of disagreement between Bayer Crop Science (BCS) and the PPR Panel is the interpretation of morphometric data. BCS contends that imidacloprid caused no morphometric effects in their DNT study; meanwhile BCS recognizes that their morphometric investigations were limited to the high dose and control groups. By contrast, the PPR Panel considered the morphometric data a source of concern and the lack of intermediate and low dose data as important missing information. Using the available data it is impossible to assess a dose-response relationship for morphometric changes. The level of uncertainty identified in brain morphometry precludes a robust characterization of the DNT potential of imidacloprid.

This study aimed to better elucidate reproductive and possible hormonal effects of the fungicide carbendazim (CBZ) through a review of published toxicological studies as well as an evaluation of this fungicide in the Hershberger and uterotrophic assays, which are designed to detect in vivo effects of the sex hormones. The literature review indicates that CBZ induces reproductive and developmental toxicity through alteration of many key events which are important to spermatogenesis. The lower dose of CBZ (100 mg/kg) evaluated in the Hershberger test increased prostate weight compared to control group but did not alter the weight of other testosterone-dependent tissues. In the uterotrophic assay, CBZ did not induce an estrogenic or an antiestrogenic effect. In the literature, it has been reported that CBZ may: 1) alter the levels of various hormones (testosterone, LH, FSH, GnRH); 2) negatively influence testicular steroidogenesis; 3) have androgenic effects acting directly in the androgenic receptors and/or increasing the expression of androgen receptors. Despite the contradictory results reported by the different studies that investigated a possible endocrine mode of action of CBZ, it seems that this fungicide may influence the hypothalamus-pituitary-gonad axis in addition to being a testicular toxicant.

The editor of Food and Chemical Toxicology (FCT) uses double standards when it comes to publishing in favour of the industry, Prof. Séralini’s team say. Now the journal’s publisher Elsevier has compelled him to publish a right of reply by the Séralini team. More than a year after its publication, the editor of Food and Chemical Toxicology (FCT), Dr A. Wallace Hayes, retracted the long-term toxicity study on two Monsanto products, the NK603 GM maize and its associated herbicide Roundup by Séralini et al. He did so despite the fact that he found neither fraud nor conscious misinterpretation in the study. In a new article published in FCT, following pressure from the journal’s publisher Elsevier, the scientists explain why they do not accept Dr Hayes’ conclusion. They denounce the lack of scientific validity of the reasons given for the reatraction, explain why the Sprague-Dawley rat strain used is appropriate, and describe the statistical results in depth concerning the blood and urine parameters affected, proving that the liver and kidney pathologies and the mammary tumours are solidly based.

Single dose of imidacloprid (IMI-20 mg/kg bodyweight) was orally administered in female rats. Its disposition along with two metabolites 6-chloro nicotinic acid (6-CNA) and 6-hydroxy nicotinic acid (6-HNA) was monitored in organs (brain, liver, kidney, and ovary) and bodily fluids (blood, urine) at 6, 12, 24 and 48 h and faeces at 24 and 48 h. Maximum concentration (Cmax) of IMI and metabolites in each organ and bodily fluid occurred after 12 h. Area under curve (AUC) of IMI ranged from 35 to 358 μg/ml/h; 6-CNA: 27.12–1006.42 μg/ml/h and 6-HNA: 14.98–302.74 μg/ml/h in different organs and bodily fluids. Clearance rate of IMI was maximum in ovary followed by kidney, liver, brain, faeces, blood and urine. Percent inhibition of acetyl-cholinesterase (AChE) was comparable in brain and Red Blood Cells (RBC) at 6–48 h which suggests the RBC-AChE as valid biomarker for assessing IMI exposure. It is evident that IMI was absorbed, metabolized, and excreted showing increased level of serum enzymes like Glutamic oxaloacetic transaminase (GOT), Glutamic pyruvic transaminase (GPT) and biochemical constituents like billirubin and Blood Urea Nitrogen (BUN) at 48 h. These data suggest that IMI is widely distributed, metabolized and induced toxicology effects at 20 mg/kg bodyweight to female rats.

During the neurodevelopmental period, the brain is potentially more susceptible to environmental exposure to pollutants. The aim was to determine if neonatal exposure to permethrin (PERM) pesticide, at a low dosage that does not produce signs of obvious abnormalities, could represent a risk for the onset of diseases later in the life.