CHRONIC NITRIC-OXIDE SYNTHASE INHIBITION AGGRAVATES GLOMERULAR INJURY IN RATS WITH SUBTOTAL NEPHRECTOMY

Besides its glomerular hemodynamic effects, nitric oxide (NO) inhibits platelet aggregation and mesangial cell proliferation, two mechanisms possibly involved in the pathogenesis of glomerulosclerosis (GS). Chronic NO synthase inhibition in the rat leads to marked arterial hypertension and promotes glomerular and interstitial injury, but only mild GS. In this study, NO synthase blockade by nitro-L-arginine methyl ester (L-NAME) was associated with 5/6 nephrectomy, a well-known model of GS. Sixty-eight adult male Munich-Wistar rats were distributed among four groups: SHAM (no renal ablation or drug treatment), NX (5/6 nephrectomy), NX+NAME (5/6 nephrectomy and chronic treatment with L-NAME, 5 mg/dL in drinking water) and NX+NAME+L (as in group NX+NAME but also receiving the angiotensin II receptor inhibitor Losartan potassium (L), 25 mg/dL in drinking water), One week after ablation, rats of Group NX showed moderate glomerular hypertension and hypertrophy. Although glomerular enlargement was also modest in Group NX+NAME, glomerular hypertension was particularly severe in this group. Both alterations were absent in Group NX+NAME+L. Only incipient glomerular and interstitial injury occurred at this phase. Three weeks after ablation, renal structural injury was still modest in Group NX. By contrast, Group NX+NAME exhibited marked GS, glomerular ischemic injury, interstitial expansion, and creatinine retention. Renal injury was largely prevented in Group NX+NAME+L, Tuft enlargement occurred in all groups but was most prominent in Group NX. NO synthase inhibition aggravates parenchymal injury and functional impairment in the remnant kidney by mechanisms that may involve glomerular hypertension and renin-angiotensin activation but that appear to be unrelated to glomerular enlargement.571498150

The Unquantified Risk of Post-Fire Metal Concentration in Soil: a Review

Forest fire is a natural disturbance that occurs in many terrestrial ecosystems specifically in the semi-arid environments and is considered to be an important cause of environmental change. Though many causes of fire are identified, including lightning, volcanic eruption, power line sparks, etc., human involvement is the most significant factor. Fire events are able to alter the physical, chemical and biogeochemical properties of the soil and surface materials and are able to release major and trace metals into the environment. This may be more significant in mining-affected and industrial landscapes, where elevated concentrations of metals present in the soil. After the fire event, metals become more mobile due to the increase in soil surface exposure and the mobility associated with ash dispersal. This mobility may increase the bioavailability of the metals, which may generate water quality issues and may contribute to human and environmental health concerns. Even though, the influences of fire on many soil properties are well established, the behaviour of metals with respect to fire is not well investigated. However, a few studies report that major and trace metals include Cd, Cr, Co, Cu, Hg, Mn, Ni, Pb, Zn and As are mobilized after fire with increased concentrations in soil and water resources and this might pose a risk to human health and ecosystems. Climate change may increase the intensity, frequency and areal extend of fire events and hence increase the metal concentrations and their potential health impacts. This paper reviews post-fire (wild fire) mobility of metals in soil common in contaminated forest ecosystems. The human and ecological health risks of these metals are also considered. © 2017, Springer International Publishing Switzerland