RESUMO
Inorganic arsenic is an environmental carcinogen.Chronic exposure to inorganic arsenic has also been suggested being associated with diabetes mellitus and cardiovascular disease, which is a prominent feature of glycolipid metabolism disorders. This article describes the current findings from epidemiological studies on arsenic exposure and diabetes and cardiovascular disease, as well as the possible mechanisms underlying the regulation of glycolipid metabolism after arsenic exposure. It is demonstrated that the effect of arsenic exposure on glycolipid metabolism is mediated through multiple mechanisms that are interrelated, rather than by a single mechanism, eventually leading to diabetes mellitus and cardiovascular disease.
RESUMO
Thioredoxin (TRX) is an important component in the thioredoxin system which is comprised of TRX,thioredoxin reductase (TRXR),and reduced coenzyme Ⅱ (NADPH).TRX is widely expressed in nearly all living cells and functions as protein disulfide reductase involving in many important biological processes,including redox signaling,the inhibition of apoptosis,regulation of transcription factors,and immune responses.TRX plays an important role in the regulation of the intracellular redox state against oxidative stress.Epidemiological studies showed that high arsenic exposure led to significant increases of serum levels of reactive oxygen species and decreases of antioxidant levels.Liver cell injury induced by arsenic via oxidative stress has been extensively studied.Oxidative stress in the process of lipid peroxidation has been widely recognized as one of the main mechanisms of arsenic poisoning.This process can produce a variety of free radicals and non-radical products those cause liver cell dysfunction or directly attack liver cells causing liver damage.Therefore,we hypothesized that TRX could play an important protective role in arsenic-induced liver injury.This paper reviews the antioxidative role of TRX in the liver injury caused by arsenic poisoning.
RESUMO
Thioredoxin (TRX) is an important component in the thioredoxin system which is comprised of TRX,thioredoxin reductase (TRXR),and reduced coenzyme Ⅱ (NADPH).TRX is widely expressed in nearly all living cells and functions as protein disulfide reductase involving in many important biological processes,including redox signaling,the inhibition of apoptosis,regulation of transcription factors,and immune responses.TRX plays an important role in the regulation of the intracellular redox state against oxidative stress.Epidemiological studies showed that high arsenic exposure led to significant increases of serum levels of reactive oxygen species and decreases of antioxidant levels.Liver cell injury induced by arsenic via oxidative stress has been extensively studied.Oxidative stress in the process of lipid peroxidation has been widely recognized as one of the main mechanisms of arsenic poisoning.This process can produce a variety of free radicals and non-radical products those cause liver cell dysfunction or directly attack liver cells causing liver damage.Therefore,we hypothesized that TRX could play an important protective role in arsenic-induced liver injury.This paper reviews the antioxidative role of TRX in the liver injury caused by arsenic poisoning.