Impact of Land Degradation on Soil Microbial Biomass and Activity in Northeast Brazil

Land degradation causes great changes in the soil biological properties. The process of degradation may decrease soil microbial biomass and consequently decrease soil microbial activity. The study was conducted out during 2009 and 2010 at the four sites of land under native vegetation (NV), moderately degraded land (LDL), highly degraded land (HDL) and land under restoration for four years (RL) to evaluate changes in soil microbial biomass and activity in lands with different degradation levels in comparison with both land under native vegetation and land under restoration in Northeast Brazil. Soil samples were collected at 0-10 cm depth. Soil organic carbon (SOC), soil microbial biomass C (MBC) and N (MBN), soil respiration (SR), and hydrolysis of fluorescein diacetate (FDA) and dehydrogenase (DHA) activities were analyzed. After two years of evaluation, soil MBC, MBN, FDA and DHA had higher values in the NV, followed by the RL. The decreases of soil microbial biomass and enzyme activities in the degraded lands were approximately 8-10 times as large as those found in the NV. However, after land restoration, the MBC and MBN increased approximately 5-fold and 2-fold, respectively, compared with the HDL. The results showed that land degradation produced a strong decrease in soil microbial biomass. However, land restoration may promote short- and long-term increases in soil microbial biomass.

Enzyme activity in the small intestine of goat kids during the period of passive immunity acquisition

Enzyme activity of protein and carbohydrate degradation in small intestinal mucosa was investigated in goat kids fed with lyophilized bovine and goat colostrum. At 0,7 and 14 h of life 15 male newborns received 5% of body weight of lyophilized bovine colostrum and 14 goat colostrum, both with 55 mg/mL of IgG. Duodenum, jejunum and ileum samples were collected at 18,36 and 96 h of life. Three animals were sampled at birth, without colostrum intake. Activity of aminopeptidase N and A, dipeptidil peptidase IV, lactase, maltase and sucrase was determined as one international unit per gram of tissue. Intracellular enzymatic activity of acid phosphatase was observed by histochemistry in tissue section. Only the activity of aminopeptidase A in the ileum was affected by treatment, with a greater value for LBC than for GC (P < 0.05). The aminopeptidase N activity was the highest at 36 h in the duodenum (P < 0.05) and lowest at 96 h in the jejunum (P < 0.05). Dipeptidil peptidase IV activity was highest at 36 h in the duodenum (P < 0.05), lowest at 96 h in the jejunum (P < 0.05) and higher at 36 h than at 96 h in the ileum (P < 0.05). Aminopeptidase A activity in the ileum was highest at 36 h (P < 0.05), followed by 18 and 96 h of life (P < 0.05). Lactase activity in the duodenum increased from 18 to 36 h and from 36 to 96 h in the jejunum (P < 0.05). Maltase activity increased only in the duodenum from 18 to 96 h (P < 0.05). Sucrase activity in the jejunum decreased from 18 to 36 h and from 36 to 96 h in the ileum (P < 0.05). At birth, activity of most enzymes was similar to that at later times (P < 0.05). Histochemistry analyses showed a higher frequency of lysosomes with acid phosphatase activity in the duodenum, especially at 36 h of life. In the jejunum, the presence of lysosomes with acid phosphatase activity was the highest at 96 h, followed by 36 and 18 h of life. In the ileum, all samples showed low presence of lysosomes with acid phosphatase activity. These results indicate that lyophilized bovine colostrum, as a heterologous source of antibodies or nutrients, is a possible alternative management tool for goats. The present work also suggests that in the first 4 days of life, enzyme activity in the intestinal epithelium of goats is still not fully stimulated, which is an important characteristic for these animals that depend on macromolecule absorption to acquire passive protection after birth. (C) 2012 Elsevier B.V. All rights reserved.

Degradation of [D-Leu]-Microcystin-LR by solar heterogeneous photocatalysis (TiO2)

The present study investigates the use of solar heterogeneous photocatalyis (TiO2) for the destruction of [D-Leu]-Microcystin-LR, powerful toxin of widespread occurrence within cyanobacteria blooms. We extracted [D-Leu]-Microcystin-LR from a culture of Microcystis spp. and used a flat plate glass reactor coated with TiO2 (Degussa, P25) for the degradation studies. The irradiance was measured during the experiments with the aid of a spectroradiometer. After the degradation experiments, toxin concentrations were determined by HPLC and mineralization by TOC analyses. Acute and chronic toxicities were, quantified using mice and phosphatase inhibition in vitro assays, respectively. According to the performed experiments, 150 min were necessary to reduce the toxin concentration to the WHO's guideline for drinking water (from 10 to 1 mu g L-1) and to mineralize 90% of the initial carbon content. Another important finding is that solar heterogeneous photocatalysis was a destructive process indeed, not only for the toxin, but also for the other extract components and degradation products generated. Moreover, toxicity tests using mice have shown that the acute effect caused by the initial sample was removed. However, tests using the phosphatase enzyme indicated that it may be formed products capable of inducing chronic effects on mammals. The performed experiments indicate the feasibility of using solar heterogeneous photocatalysis for treating contaminated water with [D-Leu]-Microcystin-LR, not only due to its destruction, but also to the significant removal of organic matter and acute toxicity that can be achieved. (C) 2012 Elsevier Ltd. All rights reserved.

Impact of Protease Inhibitors on Dentin Matrix Degradation by Collagenase

This proof-of-concept study assessed whether the reduction of the degradation of the demineralized organic matrix (DOM) by pre-treatment with protease inhibitors (PI) is effective against dentin matrix loss. Bovine dentin slices were demineralized with 0.87 M citric acid, pH 2.3, for 36 hrs. In sequence, specimens were treated or not (UT, untreated) for 1 min with gels containing epigallocatechin 3-gallate (EGCG, 400 A mu M), chlorhexidine (CHX, 0.012%), FeSO4 (1 mM), NaF (1.23%), or no active compound (P, placebo). Specimens were then stored in artificial saliva (5 days, 37 degrees C) with the addition of collagenase (Clostridium histolyticum, 100 U/mL). We analyzed collagen degradation by assaying hydroxyproline (HYP) in the incubation solutions (n = 5) and evaluated the dentin matrix loss by profilometry (n = 12). Data were analyzed by ANOVA and Tukey's test (p < 0.05). Treatment with gels containing EGCG, CHX, or FeSO4 led to significantly lower HYP concentrations in solution and dentin matrix loss when compared with the other treatments. These results strongly suggest that the preventive effects of the PI tested against dentin erosion are due to their ability to reduce the degradation of the DOM.

Cytoprotective role of heme oxygenase-1 and heme degradation derived end products in liver injury

The activation of heme oxygenase-1 (HO-1) appears to be an endogenous defensive mechanism used by cells to reduce inflammation and tissue damage in a number of injury models. HO-1, a stress-responsive enzyme that catabolizes heme into carbon monoxide (CO), biliverdin and iron, has previously been shown to protect grafts from ischemia/reperfusion and rejection. In addition, the products of the HO-catalyzed reaction, particularly CO and biliverdin/bilirubin, have been shown to exert protective effects in the liver against a number of stimuli, as in chronic hepatitis C and in transplanted liver grafts. Furthermore, the induction of HO-1 expression can protect the liver against damage caused by a number of chemical compounds. More specifically, the CO derived from HO-1-mediated heme catabolism has been shown to be involved in the regulation of inflammation; furthermore, administration of low concentrations of exogenous CO has a protective effect against inflammation. Both murine and human HO-1 deficiencies have systemic manifestations associated with iron metabolism, such as hepatic overload (with signs of a chronic hepatitis) and iron deficiency anemia (with paradoxical increased levels of ferritin). Hypoxia induces HO-1 expression in multiple rodent, bovine and monkey cell lines, but interestingly, hypoxia represses expression of the human HO-1 gene in a variety of human cell types (endothelial cells, epithelial cells, T cells). These data suggest that HO-1 and CO are promising novel therapeutic molecules for patients with inflammatory diseases. In this review, we present what is currently known regarding the role of HO-1 in liver injuries and in particular, we focus on the implications of targeted induction of HO-1 as a potential therapeutic strategy to protect the liver against chemically induced injury.