Valenciennes, 1830 Otolith Morphology, Age, and Growth in the Aegean Sea (E. Mediterranean).

Otoliths are important structures for balance and hearing of fish and constitute a useful tool in fisheries science. This study provides, for the first time in the Mediterranean, information on the otolith morphometrics of , collected from the South Aegean Sea, and enriches the existing information on its age and growth by sex. The otolith shape variables examined showed a more circular to square otolith shape, related to the body size.

Decline in Size-at-Maturity of European Hake in Relation to Environmental Regimes: A Case in the Eastern Ionian Sea.

European hake, L. 1758, is a highly valuable demersal fish species exploited in both the east Atlantic and the Mediterranean Sea. Changes in the size-at-maturity of this species have been reported in various geographic areas.

Feeding Habits of and the Effect of Body Size.

The feeding habits of organisms are important elements in their ecological role and are affected by several factors. The present study provides for the first time information on the diet and feeding strategy of (Valenciennes, 1830) and examines the effects of various factors on the species' feeding activity. Various indices (vacuity index, numerical and weight proportion, frequency of occurrence, alimentary coefficient, index of relative importance, diet breadth and overlap, Shannon-Wiener index, and trophic level) were estimated.

Assessment on marine litter ingested by fish in the Adriatic and NE Ionian Sea macro-region (Mediterranean).

This study presents data on the marine litter occurrence in the stomachs of fish species living in different marine habitats for the Adriatic and NE Ionian Sea macro-region. "Macro-litter" was examined in 614 specimens belonging to 11 species, while micro-litter in 230 specimens belonging to 7 species. The study highlights for the first time the presence of litter in the stomachs of the fish species Citharus linguatula.

Anthropogenic microfibres pollution in marine biota. A new and simple methodology to minimize airborne contamination.

Research studies on the effects of microlitter on marine biota have become more and more frequent the last few years. However, there is strong evidence that scientific results based on microlitter analyses can be biased by contamination from air transported fibres. This study demonstrates a low cost and easy to apply methodology to minimize the background contamination and thus to increase results validity.

Diet and feeding strategy of blackmouth catshark Galeus melastomus.

Diet and feeding strategy of the blackmouth catshark Galeus melastomus in the deep waters of the eastern Ionian Sea were investigated. Sampling was carried out using experimental bottom longline fishing at depths ranging from 300 to 855 m in summer and autumn 2010. Diet variability with fish size, season, area, sex and depth zone was tested and only season was found to significantly affect the diet of the species.

Spatial distribution and life-history aspects of blackspot seabream Pagellus bogaraveo (Osteichthyes: Sparidae).

Spatial distribution and life history aspects of Pagellus bogaraveo in the eastern Ionian Sea were investigated using the data from 13 different studies carried out in the area from 1983 to 2010. The spatial patterns of the abundance, biomass and mean size showed that the species inhabits the shallow waters of the shelf (<170 m depth) as juveniles up to a certain size (<180 mm total length, LT ), moving to deeper waters of the slope (mainly 400-500 m depth) as adults. The spatial pattern of abundance indicated a continuous distribution of the species in deep waters, with hot-spot areas of high values, whereas in shallow waters distribution was more discontinuous, with higher concentrations of juveniles in estuaries and brackish waters.

Inhibition of proteasome activity sensitizes dopamine neurons to protein alterations and oxidative stress.

Impairment in the capacity of the ubiquitin-proteasome pathway to clear unwanted proteins has been implicated in the cell death that occurs in Parkinson's disease (PD). In support of this concept, defects in proteasomal structure and function, as well as protein aggregates and increased levels of oxidized proteins are found in the substantia nigra of PD patients. We have previously demonstrated that inhibition of proteasome activity in mesencephalic cultures induces degeneration of dopaminergic neurons coupled with the formation of proteinaceous intracellular inclusions.

Levodopa in the treatment of Parkinson's disease: current controversies.

Levodopa is the most effective symptomatic agent in the treatment of Parkinson's disease (PD) and the "gold standard" against which new agents must be compared. However, there remain two areas of controversy: (1) whether levodopa is toxic, and (2) whether levodopa directly causes motor complications. Levodopa is toxic to cultured dopamine neurons, and this may be a problem in PD where there is evidence of oxidative stress in the nigra.

Alterations in the cellular distribution of bcl-2, bcl-x and bax in the adult rat substantia nigra following striatal 6-hydroxydopamine lesions.

The proteins of the bcl-2 family play an important role during apoptosis and may also regulate cell death in response to oxidative stress, which has been implicated in Parkinson's disease. In this study we examined the localization of the pro-apoptotic protein bax, and the anti-apoptotic proteins bcl-2 and bcl-x(L) in the substantia nigra (SN) of the adult rat and their response to oxidative stress caused by striatal injections of 6-hydroxydopamine (6-OHDA). Our data show that bcl-2, bcl-x and bax proteins are present in the SN.

Toxicity of glutathione depletion in mesencephalic cultures: a role for arachidonic acid and its lipoxygenase metabolites.

The contribution of arachidonic acid (AA) release and metabolism to the toxicity that results from glutathione (GSH) depletion was studied in rat mesencephalic cultures treated with the GSH synthesis inhibitor l-buthionine sulfoximine. Our data show that GSH depletion is accompanied by increased release of AA, which is phosholipase A2 (PLA2) dependent. Exogenous AA is toxic to GSH-depleted cells.

Levodopa is toxic to dopamine neurons in an in vitro but not an in vivo model of oxidative stress.

Levodopa is the "gold standard" for the symptomatic treatment of Parkinson's disease (PD). There is a theoretical concern, however, that levodopa might accelerate the rate of nigral degeneration, because it undergoes oxidative metabolism and is toxic to cultured dopaminergic neurons. Most in vivo studies do not show evidence of levodopa toxicity; levodopa is not toxic to normal rodents, nonhuman primates, or humans and is not toxic to dopamine neurons in dopamine-lesioned rodents or nonhuman primates in most studies.

Glutathione depletion and oxidative stress.

Oxidative stress is believed to contribute to the pathogenesis of Parkinson's disease. One of the indices of oxidative stress is the depletion of the antioxidant glutathione (GSH), which may occur early in the development of Parkinson's disease. To study the role of GSH depletion in the survival of dopamine neurons we treated mesencephalic cultures with the GSH synthesis inhibitor L-buthionine sulfoximine.

Lipopolysaccharide prevents cell death caused by glutathione depletion: possible mechanisms of protection.

Glutathione is an important cellular antioxidant present at high concentrations in the brain. We have previously demonstrated that depletion of glutathione in mesencephalic cultures results in cell death and that the presence of glia is necessary for the expression of toxicity. Cell death following glutathione depletion can be prevented by inhibition of lipoxygenase activity, implicating arachidonic acid metabolism in the toxic events.

Impairment of the ubiquitin-proteasome system causes dopaminergic cell death and inclusion body formation in ventral mesencephalic cultures.

Mutations in alpha-synuclein, parkin and ubiquitin C-terminal hydrolase L1, and defects in 26/20S proteasomes, cause or are associated with the development of familial and sporadic Parkinson's disease (PD). This suggests that failure of the ubiquitin-proteasome system (UPS) to degrade abnormal proteins may underlie nigral degeneration and Lewy body formation that occur in PD. To explore this concept, we studied the effects of lactacystin-mediated inhibition of 26/20S proteasomal function and ubiquitin aldehyde (UbA)-induced impairment of ubiquitin C-terminal hydrolase (UCH) activity in fetal rat ventral mesencephalic cultures.

Glial cell line derived neurotrophic factor promotes the recovery of dopamine neurons damaged by 6-hydroxydopamine in vitro.

Glial cell line derived neurotrophic factor (GDNF) has been shown to be a potent neurotrophic factor for dopamine neurons in culture and to prevent the loss of substantia nigra dopamine neurons following in vivo lesions with 6-hydroxydopamine (6-OHDA). In this study we used mesencephalic cultures containing both neurons and glia to examine whether GDNF protects dopamine neurons from 6-OHDA toxicity in vitro. Our data show that GDNF does not prevent the loss of dopamine neurons caused by treatment with 6-OHDA in vitro.

Glial cells mediate toxicity in glutathione-depleted mesencephalic cultures.

We have examined the role of glial cells in the toxicity that results from inhibition of reduced glutathione (GSH) synthesis by L-buthionine sulfoximine (BSO) in mesencephalic cell cultures. We show that GSH depletion, to levels that cause total cell loss in cultures containing neurons and glial cells, has no effect on cell viability in enriched neuronal cultures. An increase in the plating cell density sensitizes glia-containing cultures to GSH depletion-induced toxicity.

Deprenyl and desmethylselegiline protect mesencephalic neurons from toxicity induced by glutathione depletion.

Oxidative stress is thought to play an important role in the pathogenesis of Parkinson's disease (PD). Glutathione (GSH), a major cellular antioxidant, is decreased in the substantia nigra pars compacta of PD patients. The aim of the present study was to investigate whether deprenyl and its desmethyl metabolite, putative neuroprotective agents in the treatment of PD, could protect cultured rat mesencephalic neurons from cell death caused by GSH depletion due to treatment with L-buthionine-(S,R)-sulfoximine (BSO).

Basic fibroblast growth factor stimulation of glial cells protects dopamine neurons from 6-hydroxydopamine toxicity: involvement of the glutathione system.

Neurotrophic factors have been shown to support the survival and promote the recovery of injured neurons both in vivo and in vitro. Here, we investigated whether glial cell line-derived neurotrophic factor (GDNF) and basic fibroblast growth factor (bFGF) could modify the damage to dopamine (DA) neurons in mesencephalic cultures caused by the neurotoxin 6-hydroxydopamine (6-OHDA). The data show that bFGF, but not GDNF, effectively protected DA neurons from 6-OHDA toxicity.

L-(-)-desmethylselegiline, a metabolite of selegiline [L-(-)-deprenyl], protects mesencephalic dopamine neurons from excitotoxicity in vitro.

Selegiline [L-(-)-deprenyl], a monoamine oxidase B inhibitor, has been used in the treatment of Parkinson's disease as a putative neuroprotective agent. Selegiline is metabolized rapidly in the gastrointestinal tract and liver to desmethylselegiline (DMS) and methamphetamine. We have previously shown that selegiline protects dopamine neurons in mesencephalic cultures from toxicity resulting from activation of glutamate receptors.

L-deprenyl protects mesencephalic dopamine neurons from glutamate receptor-mediated toxicity in vitro.

L-Deprenyl is a relatively selective inhibitor of monoamine oxidase (MAO)-B that delays the emergence of disability and the progression of signs and symptoms of Parkinson's disease. Experimentally, deprenyl has also been shown to prevent neuronal cell death in various models through a mechanism that is independent of MAO-B inhibition. We examined the effect of deprenyl on cultured mesencephalic dopamine neurons subjected to daily changes of feeding medium, an experimental paradigm that causes neuronal death associated with activation of the NMDA subtype of glutamate receptors.

Secretion of GDNF by glial cells does not account for the neurotrophic effect of bFGF on dopamine neurons in vitro.

The neurotrophic effect of bFGF on dopamine (DA) neurons in vitro depends upon its mitogenic activity on glial cells. We examined whether glial secretion of the dopaminergic growth factor GDNF is responsible for the trophic activity of bFGF on mesencephalic DA neurons. When added with lower concentrations of bFGF, GDNF had an additive trophic effect, which disappeared at optimal bFGF concentrations.