Garlic oil as a fight against histological and oxidative stress abnormalities in Wistar rats after oral inoculation of Anisakis spp. Type II (L3) (Nematoda) / [O uso do óleo de alho na luta contra anormalidades histológicas e de estresse oxidativo em ratos Winstar após inoculação oral de Anisakis spp. Tipo II (L3) (Nematoda)]

The consumption of inadequately thermally treated fish is a public health risk due to the possible propagation of Anisakis larvae and their antigenic proteins, the causative agent of the zoonotic disease anisakidosis. The present study demonstrated the physiological and histopathological changes that accompanied an oral inoculation of crude extracts from fresh and thermally treated Anisakis Type II (L3) in Wistar albino rats. Nematode worms were isolated from the marine fish Dicentrarchus labrax. They were examined and taxonomically identified using light and scanning electron microscopy. The study was performed in 6 rat groups: a control group (I), a garlic oil (GO) inoculated group (II), a fresh L3 inoculated group (III), a thermally treated L3 inoculated group (IV), a fresh L3 + GO inoculated group (V), and a thermally treated L3 + GO inoculated group (VI). It was observed that rats inoculated with fresh and thermally treated L3 crude extracts showed abnormal oxidative stress markers associated with the destruction of normal architecture of spleen and thymus. GO produced a protective effect in rat groups inoculated with L3 extracts + GO administration via the amelioration of oxidative stress markers, which was confirmed by the marked normal structure of the organs' histology. Cooking of L3 infected fish induced severe physiological and histopathological alterations compared to uncooked infected fish. The administration of garlic before and after fish eating is recommended to avoid the dangerous effect of anisakids, even if they are cooked.(AU)

O consumo de peixes tratados termicamente de forma inadequada é um risco à saúde pública devido à possível propagação das larvas de Anisakis e suas proteínas antigênicas, o agente causador da doença zoonótica anisakidose. O presente estudo demonstrou as alterações fisiológicas e histopatológicas que acompanharam a inoculação oral de extratos brutos de Anisakis Tipo II (L3) frescos e termicamente tratados em ratos Wistar albinos. Vermes nematoides foram isolados do peixe marinho Dicentrarchus labrax e foram examinados e identificados taxonomicamente usando microscopia óptica e eletrônica de varredura. O estudo foi realizado em 6 grupos de ratos: grupo controle (I), grupo inoculado com óleo de alho (GO) (II), grupo inoculado com L3 fresco (III), grupo inoculado com L3 tratado termicamente (IV), grupo inoculado com L3 + GO fresco (V), e grupo inoculado com L3 + GO tratado termicamente (VI). Observou-se que ratos inoculados com extrato bruto L3 fresco e tratado termicamente mostraram marcadores de estresse oxidativo anormais associados à destruição da estrutura normal do baço e do timo. GO produziu um efeito protetor em grupos de ratos inoculados com extrato L3 + administração de GO através da melhoria dos marcadores de estresse oxidativo, que foi confirmada pela marcante estrutura normal da histologia dos órgãos. O cozimento de peixes infectados com L3 induziu alterações fisiológicas e histopatológicas graves quando comparado com peixes infectados não cozidos. Recomenda-se a administração de alho antes e depois da ingestão do peixe para evitar o efeito perigoso dos anisakídeos, mesmo se cozidos.(AU)

Identification of a new human mtDNA polymorphism (A14290G) in the NADH dehydrogenase subunit 6 gene

Leber's hereditary optic neuropathy (LHON) is a maternally inherited form of retinal ganglion cell degeneration leading to optic atrophy in young adults. Several mutations in different genes can cause LHON (heterogeneity). The ND6 gene is one of the mitochondrial genes that encodes subunit 6 of complex I of the respiratory chain. This gene is a hot spot gene. Fourteen Persian LHON patients were analyzed with single-strand conformational polymorphism and DNA sequencing techniques. None of these patients had four primary mutations, G3460A, G11788A, T14484C, and G14459A, related to this disease. We identified twelve nucleotide substitutions, G13702C, T13879C, T14110C, C14167T, G14199T, A14233G, G14272C, A14290G, G14365C, G14368C, T14766C, and T14798C. Eleven of twelve nucleotide substitutions had already been reported as polymorphism. One of the nucleotide substitutions (A14290G) has not been reported. The A14290G nucleotide substitution does not change its amino acid (glutamic acid). We looked for base conservation using DNA star software (MEGALIGN program) as a criterion for pathogenic or nonpathogenic nucleotide substitution in A14290G. The results of ND6 gene alignment in humans and in other species (mouse, cow, elegans worm, and Neurospora crassa mold) revealed that the 14290th base was not conserved. Fifty normal controls were also investigated for this polymorphism in the Iranian population and two had A14290G polymorphism (4 percent). This study provides evidence that the mtDNA A14290G allele is a new nonpathogenic polymorphism. We suggest follow-up studies regarding this polymorphism in different populations.