Role of NF-κB/IL-1β Pathway and Caspase 3 in Mediating the Hepatoprotective Effect of Rutin against Paraquat-Induced Liver Toxicity in Male Rats

One of the most common bipyridinium herbicides that can lead to liver toxicity is paraquat. Rutin is a bioflavonoid with antioxidant, anti-inflammatory, anti-hepatotoxic, and antimicrobial properties. The effect of rutin on paraquat-induced liver toxicity was examined in this study. 48 male rats were divided into six groups: the control group was given a normal diet; the non-treated group was given paraquat; the positive control group was given paraquat, and silymarin and the treatment groups were given paraquat and rutin at doses of 25, 50, and 100 mg/kg. After fourteen days, the rats were anesthetized by xylazine-ketamine, and fasting blood samples were obtained from their hearts to measure alkaline phosphatase (ALP), aspartate transaminase (AST), alanine transaminase (ALT), malondialdehyde (MDA), creatinine, lipid profile, antioxidant capacity, and carbonyl protein. The liver tissue was removed to measure the levels of catalase (CAT), superoxide dismutase (SOD), total protein, vitamin C, plus NF-κB, IL1β, and caspase-3 gene expressions. Paraquat gavage in the untreated group (group 2) for 14 days in comparison with the control group induced a significant augmentation (p<0.05) in levels of lipid profile, AST, ALP, ALT, MDA, carbonyl protein, and also NF-κB, IL1β, Caspase3 expressions. Treatment with rutin reduced the factors as mentioned above. Paraquat poisoning induced a substantial decline (p<0.05) in HDL content, FRAP level, CAT, and SOD activity of the liver compared to the control group. However, rutin oral treatment led to a substantial increase (p<0.05) in the level of these factors compared to the paraquat-only treated group. Based on the findings of the present study, it was found that rutin can be significantly effective in improving hepatotoxicity caused by paraquat.     

Spatial and technological variability in the carbon footprint of durum wheat production in Iran

Purpose

The purpose of this study was to quantify the spatial and technological variability in life cycle greenhouse gas (GHG) emissions, also called the carbon footprint, of durum wheat production in Iran.

Methods

The calculations were based on information gathered from 90 farms, each with an area ranging from 1 to 150 ha (average 16 ha). The carbon footprint of durum wheat was calculated by quantifying the biogenic GHG emissions of carbon loss from soil and biomass, as well as the GHG emissions from fertilizer application and machinery use, irrigation, transportation, and production of inputs (e.g., fertilizers, seeds, and pesticides). We used Spearman’s rank correlation to quantify the relative influence of technological variability (in crop yields, fossil GHG emissions, and N₂O emissions from fertilizer application) and spatial variability (in biogenic GHG emissions) on the variation of the carbon footprint of durum wheat.

Results and discussion

The average carbon footprint of 1 kg of durum wheat produced was 1.6 kg CO₂-equivalents with a minimum of 0.8 kg and a maximum of 3.0 kg CO₂-equivalents. The correlation analysis showed that variation in crop yield and fertilizer application, representing technological variability, accounted for the majority of the variation in the carbon footprint, respectively 76 and 21%. Spatial variation in biogenic GHG emissions, mainly resulting from differences in natural soil carbon stocks, accounted for 3% of the variation in the carbon footprint. We also observed a non-linear relationship between the carbon footprint and the yield of durum wheat that featured a scaling factor of ?2/3. This indicates that the carbon footprint of durum wheat production (in kg CO₂-eq kg^?1) typically decreases by 67% with a 100% increase in yield (in kg ha^?1 year^?1).

Conclusions

Various sources of variability, including variation between locations and technologies, can influence the results of life cycle assessments. We demonstrated that technological variability exerts a relatively large influence on the carbon footprint of durum wheat produced in Iran with respect to spatial variability. To increase the durum wheat yield at farms with relatively large carbon footprints, technologies such as site-specific nutrient application, combined tillage, and mechanized irrigation techniques should be promoted.

     

The role of miRNA-377 as a tumor suppressor in lung cancer by negative regulation of genes belonging to ErbB signaling pathway

Molecular Biology Reports - The ErbB signaling pathway plays important role in the pathogenesis of lung cancer. We explored the role of miRNA-377 as a tumor suppressor in NSCLC through silencing of...     

Analysis of Y-chromosomal short tandem repeat (STR) polymorphism in an Iranian Sadat population

The molecular genotyping of individuals and reconstruction of kinship through short and highly polymorphic DNA markers, so called short tandem repeats (STR), has become one of the important and efficient methods in anthropology studies and forensic science. Although many populations have been analyzed, no study has yet been carried out on Sadat populations who are putative descendents of Prophet Mohammad (peace be upon him). Polymorphisms of 6 Y-STR loci (DYS19, DYS385a/b, DYS389II, DYS390, DYS392, and DYS393) have been studied in an unrelated population of Sadat males. The aim of this study was to find possible similarities within Sadat males, resided in Iran. Among Sadat, DYS385b was proved to be the most polymorphic (GD = 0.8588), and DYS392 showed the lowest polymorphism (GD = 0.3527). In 50 samples, 45 different haplotypes were found, of which 39 haplotypes were unique. In the study, three samples had multi-allelic patterns. Haplotype diversity, in regard to these 7 markers was 0.9942.     

The effect of sub-lethal exposure to copper and the time course of recovery in clean water on biochemical changes in juvenile fish (Acipenser persicus)

This study reports the 96-h LC₅₀ value and tissue copper (Cu) levels and biochemical changes in juvenile fish (Acipenser persicus) exposed to 0.026?mg/l ambient Cu for 1, 7 and 14?days. It then examined the recovery of the same parameters after placing the juvenile fish in clean water for a further period of 28?days. The intestine, kidney and gill Cu levels, plasma glucose, total protein, triglyceride, cortisol, triiodothyronine and thyroxine concentrations, liver protein contents, liver catalase, superoxide dismutase (SOD) and glutathione S-transferase activities were studied. The 96-h LC₅₀ value of Cu was 0.502?mg/l for juvenile A. persicus. The results indicate that Cu exposure produced significant accumulations of Cu in gills and kidney over the treatment time. Sublethal dose of Cu resulted in a short-term increase in plasma glucose, total protein and cortisol levels that decreased with time. After the 28-day recovery phase, there were significant differences in kidney Cu levels and triglyceride concentrations as well as SOD activities between recovery fish treatments and their control groups on day 42. The 28-day recovery phase caused significant decreases in total protein levels and SOD activities of Cu-exposed fish on day 42 compared to day 14. The results suggest that 28?days are insufficient for complete recovery to Cu exposure by juveniles and a longer period would be required for full recovery. Moreover, the study showed that the recovery phase following Cu exposure could change biochemical parameters to levels that are not close to those seen during exposure or control levels.     

Mechanisms of MAdCAM-1 gene expression in human intestinal microvascular endothelial cells

Mucosal addressin cell adhesion molecule-1 (MAdCAM-1) is a homing receptor preferentially expressed on gut-associated endothelial cells that plays a central role in leukocyte traffic into the mucosal immune compartment. Although the molecular mechanisms underlying endothelial ICAM-1 or E-selectin expression have been intensively investigated, the mechanisms that regulate human MAdCAM-1 expression have not been defined. We report MAdCAM-1 gene and protein expression in primary cultures of human intestinal microvascular endothelial cells (HIMEC) that was not demonstrated in human umbilical vein endothelial cells. Similar to ICAM-1 and E-selectin expression, MAdCAM-1 gene expression in HIMEC was inducible with TNF-, IL-1, or LPS activation. However, in striking contrast to ICAM-1 and E-selectin expression, MAdCAM-1 mRNA and protein expression in HIMEC was heavily dependent on culture duration and/or cellular density, suggesting a prominent role for cell-cell interaction among these endothelial cells in the expression of the mucosal addressin. MAdCAM-1 expression was inhibited by both SN-50 (NF-B inhibitor) and LY-294002 [phosphatidylinositol 3-kinase (PI3-K) inhibitor], whereas ICAM-1 and E-selectin expression was inhibited by SN-50 but not by LY-294002. The Akt phosphorylation by TNF- or LPS was greater at higher cell density, demonstrating a pattern similar to that of MAdCAM-1 expression. NF-B activation was not affected by cellular density in HIMEC. MAdCAM-1 expression in human gut endothelial cells is regulated by distinct signaling mechanisms involving both NF-B and PI3-K/Akt. These data also suggest that PI3-K/Akt is involved in the gut-specific differentiation of HIMEC, which results in expression of the mucosal addressin MAdCAM-1. cell adhesion molecules; nuclear factor-B; phosphatidylinositol 3-kinase