Phylogenetic relationships of Pseudis and Lysapsus (Anura, Hylidae, Hylinae) inferred from mitochondrial and nuclear gene sequences

The previous uncertain placement of Lysapsus and Pseudis within the neobatrachians was recently resolved by molecular and morphological studies, which supported them as members of the Hylinae subfamily. Their inter- and intrageneric relationships, however, have long been under debate and no studies shed light on these questions. Aiming to elucidate such questions, this paper used 3.2 kb comprising the mitochondrial genes 12S, tRNA valine, 16S and cytochrome b, and the nuclear exon 1 coding for rhodopsin, to all representatives of both genera (except to two subspecies of Pseudis paradoxa). The results identified three major clades: the clade 1 was composed by Lysapsus species and subspecies; clade 2 included the subspecies of the Pseudis paradoxa (Pseudis paradoxa paradoxa, P. paradoxa platensis and P. paradoxa occidentalis), P. fusca, P. bolbodactyla and P. tocantins, and clade 3 was composed by Pseudis southern Brazil species (Pseudis cardosoi and P. minuta). As closely related taxa we found Pseudis minuta + P. cardosoi; P. tocantins + P. fusca, and the subspecies within each genus. Evidence that Pseudis is not monophyletic with respect to Lysapsus was found and we suggest Lysapsus to be a junior synonym of Pseudis. Based on pair-wise comparison among gene sequences, we also suggest that the subspecies of Pseudis paradoxa and Lysapsus limellum must be considered as full species. (c) the Willi Hennig Society 2007.

A phylogenetic analysis of Pleurodema (Anura: Leptodactylidae: Leiuperinae) based on mitochondrial and nuclear gene sequences, with comments on the evolution of anuran foam nests

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Mitochondrial DNA of Nellore and European x Nellore crossing cattle of high performance

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Mitochondrial DNA variation in wild populations of Leporinus elongatus from the Paraná River basin

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Exploitation of mitochondrial nad6 as a complementary marker for studying population variability in Lepidoptera

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Primary myiasis in dog caused by Phaenicia eximia (Diptera: Calliphoridae) and preliminary mitochondrial DNA analysis of the species in Brazil

A case of primary myiasis in a dog caused by Phaenicia eximia (Robineau-Desvoidy) in Brazil is presented. A young and healthy female dog, Canis familiaris, approximate to 10 d old and still under maternal care, was found to have several eggs and Is: instars larvae in its abdomen and urogenital regions. Samples were collected in Campinas, São Paulo, and transferred to the laboratory for rearing and identification. A comparative analysis of the mitochondrial DNA (mtDNA) with 12 restriction enzymes in 2 sampled populations of P. eximia collected in different hosts (live dog and bovine carcass) and in the same locality revealed that 4, EcoRI, EcoRV, HaeIII, and MspI were suitable for detecting mtDNA markers in the 2 populations.

Dehydromonocrotaline inhibits mitochondrial complex 1. A potential mechanism accounting for hepatotoxicity of monocrotaline

Monocrotaline is a pyrrolizidine alkaloid present in plants of the Crotalaria species, which causes cytotoxicity and genotoxicity, including hepatotoxicity in animals and humans. It is metabolized by cytochrome P-450 in the liver to the alkylating agent dehydromonocrotaline. We evaluated the effects of monocrotaline and its metabolite on respiration, membrane potential and ATP levels in isolated rat liver mitochondria, and on respiratory chain complex I NADH oxidase activity in submitochondrial particles. Dehydromonocrotaline, but not the parent compound, showed a concentration-dependent inhibition of glutamate/malate-supported state 3 respiration (respiratory chain complex 1), but did not affect succinate-supported respiration (complex II). Only dehydromonocrotaline dissipated mitochondrial membrane potential, depleted ATP, and inhibited complex I NADH oxidase activity (IC50 = 62.06 mu M) through a non-competitive type of inhibition (K-I = 8.1 mu M). Therefore, dehydromonocrotaline is an inhibitor of the activity of respiratory chain complex I NADH oxidase, an action potentially accounting for the well-documented monocrotaline's hepatotoxicity to animals and humans. The mechanism probably involves change of the complex I conformation resulting from modification of cysteine thiol groups by the metabolite. (c) 2007 Elsevier Ltd. All rights reserved.

Comparative effects of lantadene A and its reduced metabolite on mitochondrial bioenergetics

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Dehydromonocrotaline induces cyclosporine A-insensitive mitochondrial permeability transition/cytochrome c release

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Aromatic antiepileptic drugs and mitochondrial toxicity: Effects on mitochondria isolated from rat liver

Idiosyncratic hepatotoxicity is a well-known complication associated with aromatic antiepileptic drugs (AAED), and it has been suggested to occur due to the accumulation of toxic arene oxide metabolites. Although there is clear evidence of the participation of an immune process, a direct toxic effect involving mitochondria dysfunction is also possible. The effects of AAED on mitochondrial function have not been studied yet. Therefore, we investigated, in vitro, the cytotoxic mechanism of carbamazepine (CB), phenytoin (PT) and phenobarbital (PB), unaltered and bioactivated, in the hepatic mitochondrial function. The murine hepatic microsomal system was used to produce the anticonvulsant metabolites. All the bioactivated drugs (CB-B, PB-B, PT-B) affected mitochondrial function causing decrease in state three respiration, RCR, ATP synthesis and membrane potential, increase in state four respiration as well as impairment of Ca(2+) uptake/release and inhibition of calcium-induced swelling. As an unaltered drug, only PB, was able to affect mitochondrial respiration (except state four respiration) ATP synthesis and membrane potential; however, Ca(2+) uptake/release as well as swelling induction were not affected. The potential to induce mitochondrial dysfunction was PT-B > PB-B > CB-B > PB. Results suggest the involvement of mitochondrial toxicity in the pathogenesis of AAED-induced hepatotoxicity. (C) 2008 Elsevier Ltd. All rights reserved.

A single multiplex PCR and SNaPshot minisequencing reaction of 42 SNPs to classify admixture populations into mitochondrial DNA haplogroups

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)