Ecological feedback mechanisms and variable disturbance regimes: the uncertain future of Mediterranean macroalgal forests.

Loss of algal canopies can result in a shift towards a turf-dominated state, where variability in species life-history traits can determine new mechanisms of feedback, and influence the degraded system under variable regimes of disturbance. By focusing on rockpools dominated by Cystoseira brachycarpa, we tested the hypothesis that the alga Dictyopteris polypodioides could take advantage of extreme regimes of disturbance related to storms, and outcompete other turfs through a distinctive combination of life traits. Replacement of the canopy was initially driven by a mix of taxon-specific life-traits and resulting assemblages were susceptible to intense events of disturbance. Subsequently, D. polypodioides dominated removal quadrats, favored by density-dependent abilities to intercept more light and reach larger size than the rest of turf. These new positive feedbacks may contribute to maintain the modified state of the system and influence its ability to withstand extreme abiotic conditions.

Modulation of lipid homeostasis in response to continuous or intermittent high-fat diet in pigs.

A high-fat diet is known to induce atherosclerosis in animal models. Dietary factors and timing of atherogenic food delivery may affect plasma lipoprotein content composition and its potential atherogenic effect. Increasingly often, humans spend periods/days eating in a completely unregulated way, ingesting excessive amounts of food rich in oils and fats, alternating with periods/days when food intake is more or less correct. We investigate the effect on lipid homeostasis of a high-fat diet administered either continuously or intermittently. We investigated control pigs receiving standard diet (C, n=7), pigs receiving a high-fat diet every day for 10 weeks (CHF, n=5), and pigs receiving a high-fat diet every other week for 10 weeks (IHF, n=7). IHF animals were shown to have a different lipid profile compared with CHF animals, with a significant increase in high-density lipoproteins (HDL) levels with respect to C and CHF groups. CHF also showed significantly higher values of TC/HDL cholesterol compared with C and IHF. Hepatic expression analysis of genes involved in lipid homeostasis showed an increasing trend of nuclear receptor LXRα along with its target genes in the CHF group and in the IHF group, whereas SREBP2 and LDLr were significantly inhibited. A significant correlation was found between ABCA1 expression and circulating levels of HDL-C. Periodic withdrawals of a high-fat atherogenic diet compared with a regular administration results in a different adaptive response of lipoprotein metabolism, which leads to a significantly higher plasma level of HDL-C and lower TC/HDL-C.

Structural influence of isothiocyanates on expression of cytochrome P450, phase II enzymes, and activation of Nrf2 in primary rat hepatocytes.

Primary cultures of rat hepatocytes were used to investigate whether and how eight isothiocynates (ITCs) with different chemical structures (the aromatic benzyl, 4-hydroxybenzyl, phenethyl isothiocyanates and the aliphatic allyl, napin, iberin, raphasatin isothiocyanates and sulforaphane) derived from hydrolyzed glucosinolates, were able to modulate cytochrome P450 (CYP) and antioxidant/detoxifying enzymes and to activate the Nrf2 transcription factor. The aromatic ITCs at 40 µM markedly increased the transcription of CYP1A1 and 1A2 mRNA and increased the associated ethoxyresorufin O-deethylase (EROD) activity after 24 h of treatment. By contrast, the aliphatic ITCs (40 µM) decreased CYP1A1 and 1A2 transcription, together with the corresponding EROD activity. The same treatment also caused a striking and similar transcriptional repression of CYP3A2, and the corresponding benzyloxyquinoline debenzylase activity in response to all the ITCs tested. In the same culture conditions, most of the antioxidant/detoxifying enzymes were significantly up-regulated by 40µM ITCs. In particular, NAD(P)H:quinone oxidoreductase and heme oxygenase-1 were induced, although to different levels, at transcriptional, protein and/or activity levels by all the ITCs. However, glutathione S-transferase activity was not induced by the allyl, benzyl, and 4-hydroxybenzyl ITCs, glutathione reductase activity was not induced by benzyl, and 4-hydroxybenzyl ITCs and catalase activity was not induced by allyl ITC. As for the Nrf2 transcription factor, a partial translocation of its protein from the cytosol to the nucleus was revealed by immunoblotting after 1h of treatment for all the ITCs tested. The ability of ITCs to induce the antioxidant and phase II enzymes did not appear to be affected by their hydrophilicity or other structural factors. Taken together, these results show that these ITCs are effective inducers of ARE/Nrf2-regulated antioxidant/detoxifying genes and have the potential to inhibit, at least in rat liver, the bioactivation of carcinogens dependent on CYP3A2 catalysis.

Cloning and tissues expression of the pig CYP1B1 and CYP2J34.

Cytochrome P450 (CYP) 1B1 and CYP2J have been studied in various mammals, but not in pig. The sequences encoding pig CYP1B1 and CYP2J34 were isolated from liver cDNA by RACE and sequenced. The open reading frames of pig CYP1B1 showed a higher sequence homology to bovine 1B1 (89%) than to dog 1B1 (88%) or to human 1B1 (85%). On the other hand, the coding sequence of pig CYP2J34 showed a similar homology (83-85%) to CYP2J of these species. From the substrate recognition sites (SRS 1-6) analysis of the deduced proteins, it was found that the porcine CYP1B1, unlike CYP2J34, completely shared the six SRS with the bovine counterpart. RT-PCR analysis of CYP1B1 and CYP2J34 expression in ten porcine tissues revealed that CYP1B1 was principally expressed in adrenal gland, whereas CYP2J34 was predominantly expressed in small intestine. These results further support the pig as an useful model for human.

Hepatocyte population dynamics during hydrocortisone and thioacetamide treatment.

The orderly organization in a number of discrete classes of weight persists in the hepatocytes during acute and chronic poisoning with thioacetamide and during a prolonged treatment with hydrocortisone, though many striking cytological and structural changes occur in the liver. The number of hepatocyte classes decreases under hydrocortisone treatment and during acute and chronic thioacetamide poisoning, and increases during recovery after acute thioacetamide poisoning and during the late phases of chronic thioacetamide poisoning. This is due to decrements and increments in dry mass of the hepatocytes, which occur by steps, through repeated losses and additions of a constant amount of solids substantially corresponding to the class period. Such a mechanism is similar to that acting in the hepatocyte atrophy due to starvation and in the hepatocyte enlargement occurring during postnatal development. Therefore, the increment and the decrement in dry mass by defined steps takes place in the hepatocytes in both physiological and pathological conditions.