Influence of temperature on growth, development and thyroid metabolism of American bullfrog tadpoles (Lithobates catesbeianus) exposed to the herbicide tebuthiuron.

The influence of temperature (25 and 32 °C) on the negative effects of the herbicide tebuthiuron (TBU, 0, 10, 50 and 200 ng.L-1, 16 days) on thyroid function and metamorphosis of Lithobates catesbeianus tadpoles was evaluated. Metamorphosis was accelerated by TBU exposure at 25 ºC, but delayed at 32 ºC with considerable losses of body mass. T3 and T4 levels were not altered. The highest TBU concentrarion at 25 ºC increased TRâ€¯ß and DIO3 transcript levels, which is consistent with development acceleration in tadpoles. At 32 ºC TRâ€¯ß transcript levels were lower than the values recorded at 25 ºC, and those tadpoles exposed to the highest TBU concentration presented increased diameter of thyroid follicles compared to controls at same temperature. This study evidences that TBU at environmentally realistic concentrations is able to disrupt thyroidogenesis in bullfrog tadpoles, impairing their development. These effects are influenced by temperature.

Herbicides employed in sugarcane plantations have lethal and sublethal effects to larval Boana pardalis (Amphibia, Hylidae).

The increasing demand for biofuels favored the expansion of sugarcane and, as a consequence, in the consumption of pesticides in Brazil. Amphibians are subject to pesticide exposure for occurring in or around sugarcane fields, and for breeding at the onset of the rainy season when pesticide consumption is common. We tested the hypothesis that herbicides used in sugarcane crops, although employed for weed control and manipulated at doses recommended by the manufacturers, can cause lethal and sublethal effects on amphibian larvae. Boana pardalis was exposed to glyphosate, ametryn, 2,4-D, metribuzin and acetochlor which account to up to 2/3 of the volume of herbicides employed in sugarcane production. High mortality was observed following prolonged exposure to ametryn (76%), acetochlor (68%) and glyphosate (15%); ametryn in addition significantly reduced activity rates and slowed developmental and growth rates. AChE activity was surprisingly stimulated by glyphosate, ametryn and 2,4-D, and GST activity by ametryn and acetochlor. Some of these sublethal effects, including the decrease in activity, growth and developmental rates, may have important consequences for individual performance for extending the larval period, and hence the risk of dessication, in the temporary and semi-permanent ponds where the species develops. Future studies should seek additional realism towards a risk analysis of the environmental contamination by herbicides through experiments manipulating not only active ingredients but also commercial formulations, as well as interactions among contaminants and other environmental stressors across the entire life cycle of native amphibian species.

Effect of Melatonin Intake on Oxidative Stress Biomarkers in Male Reproductive Organs of Rats under Experimental Diabetes.

This study investigated the antioxidant system response of male reproductive organs during early and late phases of diabetes and the influence of melatonin treatment. Melatonin was administered to five-week-old Wistar rats throughout the experiment, in drinking water (10 µg/kg b.w). Diabetes was induced at 13 weeks of age by streptozotocin (4.5 mg/100 g b.w., i.p.) and animals were euthanized with 14 or 21 weeks old. Activities of catalase (CAT), glutathione-S-transferase (GST), glutathione peroxidase (GPx), and lipid peroxidation were evaluated in prostate, testis, and epididymis. The enzymes activities and lipid peroxidation were not affected in testis and epididymis after one or eight weeks of diabetes. Prostate exhibited a 3-fold increase in GPx activity at short-term diabetes and at long-term diabetes there were 2- and 3-fold increase in CAT and GST, respectively (p ≤ 0.01). Melatonin treatment to healthy rats caused a 47% increase in epididymal GPx activity in 14-week-old rats. In prostate, melatonin administration normalized GST activity at both ages and mitigated GPx at short-term and CAT at long-term diabetes. The testis and epididymis were less affected by diabetes than prostate. Furthermore, melatonin normalized the enzymatic disorders in prostate demonstrating its effective antioxidant role, even at low dosages.

Does counting species count as taxonomy? On misrepresenting systematics, yet again.

Recent commentary by Costello and collaborators on the current state of the global taxonomic enterprise attempts to demonstrate that taxonomy is not in decline as feared by taxonomists, but rather is increasing by virtue of the rate at which new species are formally named. Having supported their views with data that clearly indicate as much, Costello et al. make recommendations to increase the rate of new species descriptions even more. However, their views appear to rely on the perception of species as static and numerically if not historically equivalent entities whose value lie in their roles as "metrics". As such, their one-dimensional portrayal of the discipline, as concerned solely with the creation of new species names, fails to take into account both the conceptual and epistemological foundations of systematics. We refute the end-user view that taxonomy is on the rise simply because more new species are being described compared with earlier decades, and that, by implication, taxonomic practice is a formality whose pace can be streamlined without considerable resources, intellectual or otherwise. Rather, we defend the opposite viewpoint that professional taxonomy is in decline relative to the immediacy of the extinction crisis, and that this decline threatens not just the empirical science of phylogenetic systematics, but also the foundations of comparative biology on which other fields rely. The allocation of space in top-ranked journals to propagate views such as those of Costello et al. lends superficial credence to the unsupportive mindset of many of those in charge of the institutional fate of taxonomy. We emphasize that taxonomy and the description of new species are dependent upon, and only make sense in light of, empirically based classifications that reflect evolutionary history; homology assessments are at the centre of these endeavours, such that the biological sciences cannot afford to have professional taxonomists sacrifice the comparative and historical depth of their hypotheses in order to accelerate new species descriptions.

In vitro exposure to fullerene C(60) influences redox state and lipid peroxidation in brain and gills from Cyprinus carpio (Cyprinidae).

Studies concerning the impact of nanomaterials, especially fullerene (C(60) ), in fresh water environments and their effects on the physiology of aquatic organisms are still scarce and conflicting. We aimed to assess in vitro effects of fullerene in brain and gill homogenates of carp Cyprinus carpio, evaluating redox parameters. A fullerene suspension was prepared by continued stirring under fluorescent light during two months. The suspension concentration was measured by total carbon content and ultraviolet-visible spectroscopy nephelometry. Characterization of C(60) aggregates was performed with an enhanced dark-field microscopy system and transmission electronic microscopy. Organ homogenates were exposed during 1, 2, and 4 h under fluorescent light. Redox parameters evaluated were reduced glutathione and oxidized glutathione, cysteine and cystine, total antioxidant capacity; activity of the antioxidant enzymes glutathione S-transferase and glutathione reductase (GR), and lipid peroxidation (TBARS assay). Fullerene induced a significant increase (p < 0.05) in lipid peroxidation after 2 h in both organs and reduced GR activity after 1 h (gills) and 4 h (brain) and antioxidant capacity after 4 h (brain). Levels of oxidized glutathione increased in the brain at 1 h and decreased at 2 h as well. Given these results, it can be concluded that C(60) can induce redox disruption via thiol/disulfide pathway, leading to oxidative damage (higher TBARS values) and loss of antioxidant competence.

Oxidation of melatonin by singlet molecular oxygen (O2(1deltag)) produces N1-acetyl-N2-formyl-5-methoxykynurenine.

It has been shown that melatonin exhibits antioxidant properties. Chemical structures of some of the products formed by the interaction of melatonin with reactive oxygen and nitrogen species have been elucidated. Despite some evidence that the reaction of melatonin with singlet molecular oxygen (O2(1deltag)) produces N1-acetyl-N2-formyl-5-methoxykynurenine (AFMK), it has not been fully documented. In this investigation, melatonin was oxidized by photosensitization with methylene blue or by a clean chemical source of O2(1deltag), the thermodecomposition of N,N'-di(2,3-dihydroxypropyl)-1,4-naphtalenedipropanamide (DHPNO2). The resulting product was characterized by high performance liquid chromatography, coupled to electrospray ionization mass spectrometry and also by 1H, 13C and dept135 nuclear magnetic resonance spectroscopy. An isotopically labeled DHPN18O2 was also prepared and used as a chemical source of labeled 18[O2(1deltag)] to unequivocally characterize the end product. The results uncovered by this work confirm the hypothesis that oxidation of melatonin by O2(1deltag) produces AFMK.