Long-chain aliphatic wax esters isolated from the sponge Chalinula saudensis (Demospongia) along the Jeddah coast of the Red Sea

A esponja Chalinula saudensis ocorre ao longo da costa de Jeddah, Arabia Saudita, mas apenas recentemente foi isolada e identificada. No presente estudo a matéria orgânica total da esponja foi extraída por solventes e o extrato foi separado por partição sucessiva através do emprego de hexano e água, clorofórmio e água e finalmente t-butanol e água. A camada contendo clorofórmio foi então separada por cromatografia em sílica. Os resultados mostraram a presença de ésteres de quatro ácidos graxos de cadeira longa (C28H56O2, C30H60O2, C32H62O2 e C36H70O2), sendo que o segundo deles foi também identificado nos corais Millepora dichotoma e Millepora platyphylla. Não se tem evidência da presença dos demais compostos em outros organismos marinhos, embora haja relatos para ésteres semelhantes de cadeia longa, mas contendo diferentes cadeias alifáticas e diferentes pesos moleculares. Os compostos isolados em C. saudensis são geralmente ceras e sua presença na esponja tem importância não só nas rotas de biosíntese, mas servem como isolantes nas variações sazonais adversas.The sponge Chalinula saudensis, which occurs along the Jeddah coast, has only recently been isolated and identified. In this study, the total crude organic matter of the sponge was extracted by solvents. The total crude extract was further separated by partitioning it with hexane and water, then with water and chloroform, and finally with water and t-butanol. The chloroform layer was subjected to separation by preparative layer chromatography on silica. One fraction contained four long-chain fatty acid esters, C28H56O2, C30H60O2, C32H62O2 and C36H70 O2. The second ester, C30H60O2, has been identified in the fire corals Millepora dichotoma and Millepora platyphylla. The others have not previously been reported from marine organisms; however similar long-chain esters with different long aliphatic chains and with different molecular weights have been identified from other marine organisms. These compounds are normally waxy and their presence in Chalinula saudensis plays a vital role in the biosynthetic pathways. They also act as insulators against seasonal variations

Mutations in mitochondrial enzyme GPT2 cause metabolic dysfunction and neurological disease with developmental and progressive features

Mutations that cause neurological phenotypes are highly informative with regard to mechanisms governing human brain function and disease. We report autosomal recessive mutations in the enzyme glutamate pyruvate transaminase 2 (GPT2) in large kindreds initially ascertained for intellectual and developmental disability (IDD). GPT2 [also known as alanine transaminase 2 (ALT2)] is one of two related transaminases that catalyze the reversible addition of an amino group from glutamate to pyruvate, yielding alanine and α-ketoglutarate. In addition to IDD, all affected individuals show postnatal microcephaly and ∼80% of those followed over time show progressive motor symptoms, a spastic paraplegia. Homozygous nonsense p.Arg404* and missense p.Pro272Leu mutations are shown biochemically to be loss of function. The GPT2 gene demonstrates increasing expression in brain in the early postnatal period, and GPT2 protein localizes to mitochondria. Akin to the human phenotype, Gpt2-null mice exhibit reduced brain growth. Through metabolomics and direct isotope tracing experiments, we find a number of metabolic abnormalities associated with loss of Gpt2. These include defects in amino acid metabolism such as low alanine levels and elevated essential amino acids. Also, we find defects in anaplerosis, the metabolic process involved in replenishing TCA cycle intermediates. Finally, mutant brains demonstrate misregulated metabolites in pathways implicated in neuroprotective mechanisms previously associated with neurodegenerative disorders. Overall, our data reveal an important role for the GPT2 enzyme in mitochondrial metabolism with relevance to developmental as well as potentially to neurodegenerative mechanisms.National Institute of Neurological Diseases and Stroke (U.S.) (R01NS035129)United States. National Institutes of Health (R21TW008223)National Cancer Institute (U.S.) (R01CA157996

Fecal sterols and pahs in sewage polluted marine environment along the eastern Red Sea coast, South of Jeddah, Saudi Arabia

404-410Water and sediment samples were takes near the sewage discharge point on the eastern Red Sea Coast of Jeddah and analyzed for PAH and fecal sterols like coprostanol, cholesterol and cholestanol. PAH were estimated spectrofluorometrically and then further analyzed by GC-MS. Sterols were derivatized by BSTFA into their corresponding trimethyl silyl derivatives and then analyzed by gas chromatography and quantified with standard sterols. PAH ranged from 1.5 to 6.5 g 1-1 in eight stations. Concentration of coprostanol in water samples showed a maximum of 8.2 g 1-1 at station XVIII and minimum 0.1 g 1-1 at station 10C. The analysis of the sediment samples indicated much higher values for fecal sterols. It was found to be 785 g 1-1 in sediment and 6.5 g 1-1 in the water samples at station XVIII. PAH did not show any distinct increase in the sediment samples. According to Grimaldt equation the value of r* (5 / 5 + 5) was determined. Out of a total of sixteen samples, fourteen samples had a value of 0.7 or higher than 0.7. This indicate a definite and a positive sewage contamination infecting almost the whole area studied. The GC-MS of the PAH indicate the presence of phenanthrene, benzophenone and 2,4-diisoprophyl naphthalene, methylnaphthalene, and 9-H-methylene flourene. Present study infers that the sewage; either untreated or partially treated is dumped into the sea