RESUMO
Soil zinc (Zn) plays a crucial role in plant growth, but excessive accumulation in the environment may lead to air, water and soil pollution. It is affected by various chemical, environmental and spatial factors. Therefore, it is important to identify the factors influencing Zn content in the landscape. The main motivation for this study is to determine the suitability of a generalized additive model (GAM) to describe change in soil Zn content due to influencing factors. A total of 1497 soil nutrient samples were collected in Fangshan District, Beijing, China. Organic matter (OM), available phosphorus (AP), available potassium (AK), alkali-hydrolyzed nitrogen (AHN) and slowly available potassium (SAK) are considered. The relationship between Zn, nutrients and geographic location (latitude & longitude) is investigated using the GAM. More precisely, the Akaike information criterion (AIC) is used to select influencing factors on Zn content and cross-validated to avoid overfitting of the multivariate model. The results show that Zn content reaches its maximum at latitude 39.8°N and longitude 115.9°E. Zinc content increases as AP increases to 150 mg/kg. When OM content is greater than 90 g/kg, Zinc content decreases with an increase in OM content. Factors that affected Zn content, in descending order of significance derived from deviance explained and adjustment coefficient of determination (Adj.R2) were AP, latitude, AHN, AK and OM. Moreover, the interactions between latitude and longitude, AHN and AP, OM and AK have significant impact on Zn.
RESUMO
Growth arrest DNA damage-inducible 153 (GADD153) expression was increased in 1-methyl-4-phenyl-pyridinium (MPP(+))-treated human SH-SY5Y neuroblastoma cells as determined by gene microarray analysis. GADD153 expression increased after 24 hr of MPP(+) (1 mM) exposure and preceded activation of caspase 3. Comparison of GADD153 expression among cultures treated with other toxins whose primary mode of action is either via mitochondrial impairment (rotenone) or via oxidative stress (6-hydroxydopamine or hydrogen peroxide) showed that GADD153 was uniquely up-regulated by MPP(+). Together these data suggest that a cellular mechanism distinct from mitochondrial impairment or oxidative stress contributes significantly to the up-regulation of GADD153 by MPP(+) and that GADD153 may function as an inducer of apoptosis following MPP(+) exposure. Published 2002 Wiley-Liss, Inc.
