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Aim: To assess the effects of L‐arginine (L‐Arg) supplementation on pulmonary oxidative stress and antioxidant defenses in rats after exhaustive exercise. Methods: Rats were randomly divided into four groups: sedentary control (SC), sedentary control with L‐Arg treatment (SC+Arg), exhaustive exercise with control diet (E) and exhaustive exercise with L‐Arg treatment (E+Arg). Rats in groups SC+Arg and E+Arg received a 2%L‐Arg diet. Rats in groups E and E+Arg underwent an exhaustive running test on a motorized treadmill. Pulmonary oxidative stress indices [xanthine oxidase (XO), myeloperoxidase (MPO), and malondialdehyde (MDA)] and antioxidant defense systems [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione reductase (GR), and glutathione (GSH)] were investigated in this study. Results: L‐Arg supplementation significantly reduced exercise‐induced elevations of XO and MPO activities in lung. L‐Arg reversed the exercise‐induced increase in SOD and GR activities, but increased CAT and GPX activities. L‐Arg administration also significantly increased the GSH levels in plasma. Conclusion: L‐Arg supplementation can prevent elevations of XO and MPO activities in the lung and favorably influence pulmonary antioxidant defense systems after exhaustive exercise.

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Long-term ethanol consumption significantly can increase jejunal lipase and decrease jejunal disaccharidase activities in both male and female rats.

AIM:To better clarify the main target organs of dimethylarsinic acid toxicity and the role of metallothionein (MTs) in modifying dimethylarsinic acid (DMAA) toxicity. METHODS:MT-I/II null (MT -/-) mice and the corresponding wild-type mice (MT +/+ ), six in each group, were exposed to DMAA (0-750 mg/kg body weight) by a single oral injection. Twenty four hours later, the lungs, livers and kidneys were collected and undergone pathological analysis, induction of apoptotic cells as determined by TUNEL and MT concentration was detected by radio-immunoassay. RESULTS:Remarkable pathological lesions were observed at the doses ranging from 350 to 750 mg/kg body weight in the lungs, livers and kidneys and MT +/+ mice exhibited a relatively slight destruction when compared with that in dose matched MT -/-mice. The number of apoptotic cells was increased in a dose dependent manner in the lungs and livers in both types of mice. DMAA produced more necrotic cells rather than apoptotic cells at the highest dose of 750 mg/kg, however, no significant increase was observed in the kidney. Hepatic MT level in MT +/+ mice was significantly increased by DMAA in a dose-dependent manner and there was no detectable amount of hepatic MT in untreated MT -/-mice. CONCLUSION:DMAA treatment can lead to the induction of apoptosis and pathological damage in both types of mice. MT exhibits a protective effect against DMAA toxicity.