Assessment of the impacts of climate change and variability on water resources and use,food security,and economic welfare in Iran

Climate change influences the agricultural sector by reducing available water resources, thereby influencing income, consumer and producer surplus, and crop prices. So, it is necessary to have a comprehensive integrated method to measure the effects of these changes on natural resources and social conditions. The present study aims to use the positive mathematical programming method to discover the trend and conditions of groundwater resources, agricultural water use, food security, and economic welfare of the agricultural sector in Iran. To this end, data for the period 2000–2015 was used under four different scenarios of normal climate change, climate change, climate variability, and concurrent climate change The results showed that the mean agricultural water use will amount to 35,103.6, 26,533.8, 35,216, and 26,510.7 million m³ and the mean decline in the reserves of aquifers will amount to 4422.22, 11,165.6, 4438.25, and 11,267.4 million m³ under the scenarios, respectively. With respect to food security, the net farm revenue will be 314,560, 248,753, 315,427, and 248,574 billion IRR, respectively. The mean crop price per ton will reach 905.3, 1141.8, 904, and 1142.8 million IRR, respectively. The mean consumer surplus will be 172,107.7, 166,450, 172,024, and 166,403 billion IRR and the mean producer surplus will be 419,959.2, 395,380, 419,751, and 395,204 billion IRR, respectively. Based on the results, to reduce the adverse impacts of climate change on different studied aspects, it is necessary to change policymaking in the water and agricultural sectors, especially regarding the shift from traditional agricultural water allocation to its market-based allocation and to change planting pattern.

     

Comparison of cellular and molecular cytotoxic mechanisms of Cochlodinium polykrikoides in isolated trout and rat hepatocytes

Harmful algal blooms produced by the marine ichthyotoxic dinoflagellate Cochlodinium polykrikoides are responsible for mass mortalities of wild and farmed fish globally. This study compared the cytotoxic mechanisms of C. polykrikoides total extract on both trout and rat liver hepatocytes. Trout hepatocytes were more sensitive than rat hepatocytes against C. polykrikoides extract. The effective concentration 50 after 3 hour incubation (EC50_3hr) concentrations found for C. polykrikoides extract in trout and rat hepatocytes (i.e., 50% membrane lysis in 3 hr) were Eq. 1 cell/ml and Eq. 240 cell/ml, respectively. C. polykrikoides extract exposure in both isolated trout and rat hepatocytes resulted in membrane lysis, reactive oxygen species formation, glutathione depletion, collapse of mitochondrial membrane potential, ATP depletion, increase in adenosine diphosphate (ADP)/adenosine triphosphate (ATP) ratio, cytochrome c release into the hepatocyte cytosol, and activation of caspases cascade. Trout hepatocyte toxicity was also associated with lysosomal membrane injury. Mitochondrial permeability transition in both trout and rat hepatocytes produced cytochrome c release from the mitochondrial intramembrane space into the cytosol. Thus, the cytochrome c release triggered activation of caspase-3 and apoptosis. Finally, data demonstrated that C. polykrikoides extract may induce more apoptotic phenotype in rat than trout hepatocytes, which in the latter favored predominantly necrotic mode of cell death.     

Toxicity of depleted uranium on isolated liver mitochondria: a revised mechanistic vision for justification of clinical complication of depleted uranium (DU) on liver

Depleted uranium (DU) is widely used in military anti-armor weapons. Recent evidence suggested that oxidative stress and mitochondrial dysfunction may contribute to DU-induced toxicity. However, the underlying mechanisms of DU toxicity in mitochondria are not well understood. In this study, liver mitochondria were obtained from Wistar rats treated with DU in the form of uranyl acetate (UA) (0.5, 1 or 2 mg/kg i.p.) using differential centrifugation. For in vitro experiments, control rat liver mitochondria were incubated with different concentrations of UA (50, 100 or 200 μM) for 1 hr. Mitochondrial reactive oxygen species (ROS) production, collapse of mitochondrial membrane potential, and mitochondrial swelling were examined by flow cytometry. Mitochondrial sources of ROS formation were determined using specific substrates and inhibitors. Extent of lipid peroxidation (LPO) and glutathione (GSH) oxidation, and also complex II and IV activities were detected via spectroscopy. Further, the concentration of ATP and ATP/ADP ratio was measured using luciferase enzyme and release of cytochrome c from mitochondria which was detected by ELISA kit. UA induced succinate-supported mitochondrial ROS production, elevated LPO levels, GSH oxidation, and mitochondrial complex II inhibition. UA also induced mitochondrial permeability transition and increase in cytochrome c release which subsequently disturbed oxidative phosphorylation and reduced the mitochondrial ATP concentration. Data suggest that mitochondrial oxidative stress and uncoupling of oxidative phosphorylation may play key roles in DU-induced hepatic toxicity.