Despite heavy consumption over a long period of time, only a small number of alcoholics develop alcoholic liver disease. This alludes to the possibility that other factors, besides alcohol, may be involved in the prog...Despite heavy consumption over a long period of time, only a small number of alcoholics develop alcoholic liver disease. This alludes to the possibility that other factors, besides alcohol, may be involved in the progression of the disease. Over the years, many such factors have indeed been identified, including iron. Despite being crucial for various important biological processes, iron can also be harmful due to its ability to catalyze Fenton chemistry. Alcohol and iron have been shown to interact synergistically to cause liver injury. Iron-mediated cell signaling has been reported to be involved in the pathogenesis of experimental alcoholic liver disease. Hepcidin is an iron-regulatory hormone synthesized by the liver, which plays a pivotal role in iron homeostasis. Both acute and chronic alcohol exposure suppress hepcidin expression in the liver. The sera of patients with alcoholic liver disease, particularly those exhibiting higher serum iron indices, have also been reported to display reduced prohepcidin levels. Alcohol-mediated oxidative stress is involved in the inhibition of hepcidin promoter activity and transcription in the liver. This in turn leads to an increase in intestinal iron transport and liver iron storage. Hepcidin is expressed primarily in hepatocytes. It is noteworthy that both hepatocytes and Kupffer cells are involved in the progression of alcoholic liver disease. However, the activation of Kupffer cells and TNF-α signaling has been reported not to be involved in the down-regulation of hepcidin expression by alcohol in the liver. Alcohol acts within the parenchymal cells of the liver to suppress the synthesis of hepcidin. Due to its crucial role in the regulation of body iron stores, hepcidin may act as a secondary risk factor in the progression of alcoholic liver disease. The clarification of the mechanisms by which alcohol disrupts iron homeostasis will allow for further understanding of the pathogenesis of alcoholic liver disease.展开更多
Silicon (Si) can enhance the resistance of plants to many abiotic stresses. To explore whether Si ameliorates Fe2+ toxicity, a hydroponic experiment was performed to investigate whether and how Si detoxifies Fe2+ toxi...Silicon (Si) can enhance the resistance of plants to many abiotic stresses. To explore whether Si ameliorates Fe2+ toxicity, a hydroponic experiment was performed to investigate whether and how Si detoxifies Fe2+ toxicity in rice (Oryza sativa L.) roots. Results indicated that rice cultivar Tianyou 998 (TY998) showed greater sensitivity to Fe2+ toxicity than rice cultivar Peizataifeng (PZTF). Treatment with 0.1 mmol L-1 Fe2+ inhibited TY998 root elongation and root biomass significantly. Reddish iron plaque was formed on root surface of both cultivars. TY998 had a higher amount of iron plaque than PZTF. Addition of Si to the solution of Fe treatment decreased the amount of iron plaque on root surface by 17.6% to 37.1% and iron uptake in rice roots by 37.0% to 40.3%, and subsequently restored root elongation triggered by Fe2+ toxicity by 13.5% in the TY998. Compared with Fe treatment, the addition of 1 mmol L-1 Si to the solution of Fe treatment increased xylem sap flow by 19.3% to 24.8% and root-shoot Fe transportation by 45.0% to 78.6%. Furthermore, Si addition to the solution of Fe treatment induced root cell wall to thicken. These results suggested that Si could detoxify Fe2+ toxicity and Si-mediated amelioration of Fe2+ toxicity in rice roots was associated with less iron plaque on root surface and more Fe transportation from roots to shoots.展开更多
Iron-mediated sp-sp3 C-C bond formation through the cross dehydrogenative coupling(CDC) of terminal alkynes with benzylic ethers or alkanes has been developed.The inexpensive iron salt is used as the catalyst to make ...Iron-mediated sp-sp3 C-C bond formation through the cross dehydrogenative coupling(CDC) of terminal alkynes with benzylic ethers or alkanes has been developed.The inexpensive iron salt is used as the catalyst to make this transformation environmentally benign.Iron-mediated sp-sp3 C-C bond formation through the cross dehydrogenative coupling(CDC) of terminal alkynes with benzylic ethers or alkanes has been developed.The inexpensive iron salt is used as the catalyst to make this transformation environmentally benign.展开更多
Transition-metal-salt-mediated radical reactions of fullerenes have attracted extensive attention as a new and important method for fullerene functionalization. The application of relatively cheap and easily available...Transition-metal-salt-mediated radical reactions of fullerenes have attracted extensive attention as a new and important method for fullerene functionalization. The application of relatively cheap and easily available ferric perchlorate (Fe(ClO 4 ) 3 ) to the synthesis of [60]fullerene (C 60 ) has demonstrated remarkable advantages and afforded a series of novel fullerene derivatives. In this review we present our recent progress in this area and summarize the reactions of C 60 with malonate esters, β-keto esters, nitriles, aldehydes/ketones, and arylboronic acids in the presence of Fe(ClO 4 ) 3 to afford the C 60-fused disubstituted lactones, C 60-fused hemiketal, C 60-fused dihydrofuran, C 60-fused oxazoles, C 60-fused 1,3-dioxolanes, and fullerenyl boronic esters. The possible reaction mechanisms for the above-mentioned reactions are also described in detail.展开更多
基金Supported by Grants from the Alcoholic Beverage Medical Research Foundation, Redox Biology Center, University of Nebraska-Lincoln, 2P20RR017675NIH grant, R01AA017738-01 to DHF
文摘Despite heavy consumption over a long period of time, only a small number of alcoholics develop alcoholic liver disease. This alludes to the possibility that other factors, besides alcohol, may be involved in the progression of the disease. Over the years, many such factors have indeed been identified, including iron. Despite being crucial for various important biological processes, iron can also be harmful due to its ability to catalyze Fenton chemistry. Alcohol and iron have been shown to interact synergistically to cause liver injury. Iron-mediated cell signaling has been reported to be involved in the pathogenesis of experimental alcoholic liver disease. Hepcidin is an iron-regulatory hormone synthesized by the liver, which plays a pivotal role in iron homeostasis. Both acute and chronic alcohol exposure suppress hepcidin expression in the liver. The sera of patients with alcoholic liver disease, particularly those exhibiting higher serum iron indices, have also been reported to display reduced prohepcidin levels. Alcohol-mediated oxidative stress is involved in the inhibition of hepcidin promoter activity and transcription in the liver. This in turn leads to an increase in intestinal iron transport and liver iron storage. Hepcidin is expressed primarily in hepatocytes. It is noteworthy that both hepatocytes and Kupffer cells are involved in the progression of alcoholic liver disease. However, the activation of Kupffer cells and TNF-α signaling has been reported not to be involved in the down-regulation of hepcidin expression by alcohol in the liver. Alcohol acts within the parenchymal cells of the liver to suppress the synthesis of hepcidin. Due to its crucial role in the regulation of body iron stores, hepcidin may act as a secondary risk factor in the progression of alcoholic liver disease. The clarification of the mechanisms by which alcohol disrupts iron homeostasis will allow for further understanding of the pathogenesis of alcoholic liver disease.
基金Supported by the National Natural Science Foundation of China (Nos. 31071847 and 31172026)the Ph.D. Programs Foundation of Ministry of Education of China (No. 20104404110016)the Foundation for High-level Talents in Higher Education of Guangdong, China
文摘Silicon (Si) can enhance the resistance of plants to many abiotic stresses. To explore whether Si ameliorates Fe2+ toxicity, a hydroponic experiment was performed to investigate whether and how Si detoxifies Fe2+ toxicity in rice (Oryza sativa L.) roots. Results indicated that rice cultivar Tianyou 998 (TY998) showed greater sensitivity to Fe2+ toxicity than rice cultivar Peizataifeng (PZTF). Treatment with 0.1 mmol L-1 Fe2+ inhibited TY998 root elongation and root biomass significantly. Reddish iron plaque was formed on root surface of both cultivars. TY998 had a higher amount of iron plaque than PZTF. Addition of Si to the solution of Fe treatment decreased the amount of iron plaque on root surface by 17.6% to 37.1% and iron uptake in rice roots by 37.0% to 40.3%, and subsequently restored root elongation triggered by Fe2+ toxicity by 13.5% in the TY998. Compared with Fe treatment, the addition of 1 mmol L-1 Si to the solution of Fe treatment increased xylem sap flow by 19.3% to 24.8% and root-shoot Fe transportation by 45.0% to 78.6%. Furthermore, Si addition to the solution of Fe treatment induced root cell wall to thicken. These results suggested that Si could detoxify Fe2+ toxicity and Si-mediated amelioration of Fe2+ toxicity in rice roots was associated with less iron plaque on root surface and more Fe transportation from roots to shoots.
基金supported by Peking University,the National Natural Science Foundation of China(20872003)National Basic Research Program of China(973 program)(2009CB825300)
文摘Iron-mediated sp-sp3 C-C bond formation through the cross dehydrogenative coupling(CDC) of terminal alkynes with benzylic ethers or alkanes has been developed.The inexpensive iron salt is used as the catalyst to make this transformation environmentally benign.Iron-mediated sp-sp3 C-C bond formation through the cross dehydrogenative coupling(CDC) of terminal alkynes with benzylic ethers or alkanes has been developed.The inexpensive iron salt is used as the catalyst to make this transformation environmentally benign.
基金supported by the National Natural Science Foundation of China (20972145, 21132007, 21102041)National Basic Research Program of China (2011CB921402)Scientific Research Foundation of Education Commission of Hubei Province (Q20120113)
文摘Transition-metal-salt-mediated radical reactions of fullerenes have attracted extensive attention as a new and important method for fullerene functionalization. The application of relatively cheap and easily available ferric perchlorate (Fe(ClO 4 ) 3 ) to the synthesis of [60]fullerene (C 60 ) has demonstrated remarkable advantages and afforded a series of novel fullerene derivatives. In this review we present our recent progress in this area and summarize the reactions of C 60 with malonate esters, β-keto esters, nitriles, aldehydes/ketones, and arylboronic acids in the presence of Fe(ClO 4 ) 3 to afford the C 60-fused disubstituted lactones, C 60-fused hemiketal, C 60-fused dihydrofuran, C 60-fused oxazoles, C 60-fused 1,3-dioxolanes, and fullerenyl boronic esters. The possible reaction mechanisms for the above-mentioned reactions are also described in detail.
