FIPRONIL AND IMIDACLOPRID REDUCE HONEYBEE MITOCHONDRIAL ACTIVITY

Bees have a crucial role in pollination; therefore, it is important to determine the causes of their recent decline. Fipronil and imidacloprid are insecticides used worldwide to eliminate or control insect pests. Because they are broad-spectrum insecticides, they can also affect honeybees. Many researchers have studied the lethal and sublethal effects of these and other insecticides on honeybees, and some of these studies have demonstrated a correlation between the insecticides and colony collapse disorder in bees. The authors investigated the effects of fipronil and imidacloprid on the bioenergetic functioning of mitochondria isolated from the heads and thoraces of Africanized honeybees. Fipronil caused dose-dependent inhibition of adenosine 5'-diphosphate-stimulated (state 3) respiration in mitochondria energized by either pyruvate or succinate, albeit with different potentials, in thoracic mitochondria; inhibition was strongest when respiring with complex I substrate. Fipronil affected adenosine 5'-triphosphate (ATP) production in a dose-dependent manner in both tissues and substrates, though with different sensitivities. Imidacloprid also affected state-3 respiration in both the thorax and head, being more potent in head pyruvate-energized mitochondria; it also inhibited ATP production. Fipronil and imidacloprid had no effect on mitochondrial state-4 respiration. The authors concluded that fipronil and imidacloprid are inhibitors of mitochondrial bioenergetics, resulting in depleted ATP. This action can explain the toxicity of these compounds to honeybees. (c) 2014 SETAC

Purinergic and glutamatergic interactions in the hypothalamic paraventricular nucleus modulate sympathetic outflow

P2X receptors are expressed on ventrolateral medulla projecting paraventricular nucleus (PVN) neurons. Here, we investigate the role of adenosine 5′-triphosphate (ATP) in modulating sympathetic nerve activity (SNA) at the level of the PVN. We used an in situ arterially perfused rat preparation to determine the effect of P2 receptor activation and the putative interaction between purinergic and glutamatergic neurotransmitter systems within the PVN on lumbar SNA (LSNA). Unilateral microinjection of ATP into the PVN induced a dose-related increase in the LSNA (1 nmol: 38 ± 6 %, 2.5 nmol: 72 ± 7 %, 5 nmol: 96 ± 13 %). This increase was significantly attenuated by blockade of P2 receptors (pyridoxalphosphate-6-azophenyl-20,40-disulphonic acid, PPADS) and glutamate receptors (kynurenic acid, KYN) or a combination of both. The increase in LSNA elicited by L-glutamate microinjection into the PVN was not affected by a previous injection of PPADS. Selective blockade of non-N-methyl-D-aspartate receptors (6-cyano-7-nitroquinoxaline-2,3-dione disodium salt, CNQX), but not N-methyl-D-aspartate receptors (NMDA) receptors (DL-2-amino-5-phosphonopentanoic acid, AP5), attenuated the ATP-induced sympathoexcitatory effects at the PVN level. Taken together, our data show that purinergic neurotransmission within the PVN is involved in the control of SNA via P2 receptor activation. Moreover, we show an interaction between P2 receptors and non-NMDA glutamate receptors in the PVN suggesting that these functional interactions might be important in the regulation of sympathetic outflow

Crystallization and preliminary X-ray diffraction analysis of selenophosphate synthetases from Trypanosoma brucei and Leishmania major

Selenophosphate synthetase (SPS) plays an indispensable role in selenium metabolism, being responsible for catalyzing the activation of selenide with adenosine 5'-triphosphate (ATP) to generate selenophosphate, the essential selenium donor for selenocysteine synthesis. Recombinant full-length Leishmania major SPS (LmSPS2) was recalcitrant to crystallization. Therefore, a limited proteolysis technique was used and a stable N-terminal truncated construct (ΔN-LmSPS2) yielded suitable crystals. The Trypanosoma brucei SPS orthologue (TbSPS2) was crystallized by the microbatch method using paraffin oil. X-ray diffraction data were collected to resolutions of 1.9 Å for ΔN-LmSPS2 and 3.4 Å for TbSPS2.

ATP, chlorophyll "a", and size structure of phytolpankton in seawater at stations in the Atlantic sector of the Southern Ocean

Chlorophyll "a" and adenozine triphosphate (ATP) concentrations together with size structure of microplankton were investigated in January-April 1989 in the Indian Ocean and in the Weddell Sea. ATP values varied from 11 to 92 ng/l, and chlorophyll "a" concentrations varied from 0.04 to 0.27 µg/l in the Indian Ocean, with prevailing nanoplankton and picoplankton fractions. Both ATP and chlorophyll "a" concentrations increased 2 times to the south of 40°S; in the Weddell Sea they exceeded 400 ng/l and 0.6 µg/l, respectively. Cells of nanophytoplankton and microphytoplankton (mainly diatoms) prevailed in size spectra. Spatial variabilities of the parameters were within one order of magnitude; their values decreased 3-4 times during 1 month. Size structure changed due to increased portion of nanoplankton and picolankton. ATP concentrations in the photic layer (0-200 m) varied from 31.96 mg/m**2 in February to 8.02 mg/m**2 in March to April. ATP concentrations were 61.5 and 98.8 mg/m**2 at depths of 4200 and 4700 m, respectively.