The use of nutrition support near the end of life for hospitalized patients with advanced cancer at a reference center: Two realities.

OBJECTIVE: To assess the frequency and factors associated of the provision of nutrition support (NS) in the last 30 days of life in patients with advanced cancer in the palliative or non-palliative setting. METHODS: Retrospective cohort study in palliative and non-palliative care units at a specialized cancer center for oncology in Brazil. The use of oral nutrition supplements (ONS) and enteral (EN) and parenteral (PN) nutrition in the 30 days before death were assessed. RESULTS: The 239 patients included were predominantly older (>60 years; 63.2%) and female (61.1%). The use of ONS was lower in palliative than non-palliative care during the last 30 (52% vs. 6%), 7 (42% vs. 4%), and 3 (23% vs. 2%) days before death (all P < .001). The use of EN and PN was lower in palliative care, decreasing with the approach of death. The independent factors associated with ONS in non-palliative care were (odds ratio): breast tumor (3.03), hypoalbuminemia (1.10), and nutrition risk (16.98); in palliative care, only the Karnofsky Performance Status (KPS) ≥40% (1.24) was associated to the use of ONS. The use of EN and PN was associated with head-neck (HN) tumor in both settings (5.41) in non-palliative and (8.74) in palliative. Others independent factors were: hypoalbuminemia (3.12) in non-palliative care and KPS (1.31) in palliative care. CONCLUSIONS: The use of NS near the end of life was high in the non-palliative and less frequent in palliative care setting. The factors associated with NS differed according to the clinical oncology setting, with one of the factors in palliative care being a better prognosis.

Diphenyl diselenide confers neuroprotection against hydrogen peroxide toxicity in hippocampal slices.

The present study aimed at investigating the potential in vitro protective effect of the organochalcogenide diphenyl diselenide - (PhSe)2 - against hydrogen peroxide (H2O2)-induced toxicity in rat hippocampal slices. Hippocampal slices were treated for 1 h with H2O2 (2 mM) in the presence or absence of (PhSe)2 (0.1-10 microM). H2O2 treatment significantly decreased cell viability (measured by MTT test) and the co-incubation with (PhSe)(2) (10 microM) significantly blunted such phenomenon. The non permeable thiol compounds dithiothreitol (DTT) (100 microM) or reduced glutathione (GSH) (100 microM), which did not display protective effects against H2O2-induced loss of cell viability per se, significantly improved the protective effects elicited by (PhSe)2. Conversely, the permeable form of GSH (GSH monoethyl ester) was unable to alter the neuroprotection mediated by (PhSe)2. The treatment of rat hippocampal slices with H2O2 also increased the lipid peroxidation and decreased the intracellular GSH levels. Moreover, (PhSe)2 (from 0.1 microM) significantly decreased H2O2-induced lipid peroxidation. Interestingly, H2O2 decreased GSH levels and this phenomenon was partially prevented by (PhSe)2. The potential effects of H2O2 on MAPKs phosphorylation (ERK1/2, p38 MAPK and JNK1/2) were also evaluated. Even though H2O2 (2 mM) did not alter p38 MAPK and JNK1/2 phosphorylation in hippocampal slices, it stimulated ERK1/2 phosphorylation and the co-incubation with (PhSe)2 (10 microM) blocked this effect. Taken together, the present results indicate that (PhSe)2 exerts protective effects against H2O2-induced oxidative damage in hippocampal slices and avoided the increase in ERK1/2 phosphorylation promoted by H2O2. The neuroprotective effect of compound seems to be related to its thiol-peroxidase-like activity and appears to occur at the extracellular milieu because a permeable form of GSH was unable to improve the protective effect of the compound as did the impermeable GSH.