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Our previous studies showed that aflatoxin B1 (AFB1) and ochratoxin A (OTA) could trigger joint immune toxicity. Little is known about the combined effects of selenomethionine (SeMet) and N-acetylcysteine (NAC) on the joint toxicities of the two toxins. In this study, results showed that SeMet or NAC alone or in combination significantly alleviated the downswing of cell viability, glutathione production, and phagorytosis induced by AFB1 and OTA in porcine alveolar macrophages. The uptrend of lactate dehydrogenase activities, apoptosis, reactive oxygen species levels, and the relative mRNA of inflammatory cytokines triggered by the two toxins was decreased. Combination of them was more effective than single application. Knockdown of p38, c-JUN N-terminal kinase (JNK), or extracellular signal-regulated kinase (ERK) via use of the corresponding specific siRNA could alleviate the joint toxicities of AFB1 and OTA. However, the ERK but not p38 or JNK pathway was involved in the protection of SeMet and NAC against the immunotoxicity. In conclusion, combination of SeMet and NAC might be a new therapeutic orientation for preventing the joint toxicities induced by AFB1 and OTA.

Selenium is an essential trace element found in vegetables as selenomethionine (SeMet) and methylselenocysteine (MeSeCys). In the present study, we used stable isotopes of Se to investigate differences between how SeMet and MeSeCys are metabolized, using methylseleninic acid (MSA) as a reference methylselenol source. A mixture containing (76)Se-SeMet, (77)Se-MeSeCys, and (82)Se-MSA (each 25 microg Se/kg b.w.) was orally administered to rats, and then, speciation analyses of Se in urine and exhaled gas were conducted using HPLC-inductively coupled plasma (ICP)-MS and GC-ICP-MS, respectively. The proportions of (76)Se-, (77)Se-, and (82)Se-selenosugar (Se-sugar) to total urinary Se metabolites originating from each tracer were very similar, while the proportion of (77)Se-tirmethylselenonium (TMSe) was much less than that of(76)Se- and (82)Se-TMSe in urine, suggesting that(77)Se-SeMet is less efficiently metabolized to TMSe. Similarly, there was significantly less (77)Se-dimethylselenide (DMSe) originating from (77)Se-SeMet than(76)Se- and (82)Se-DMSe originating from (76)Se-MeSeCys and (82)Se-MSA in exhaled gas. It is generally accepted that DMSe and TMSe are metabolites of methylselenol, a putative metabolic intermediate in Se metabolism. Methylselenol is believed to be responsible for the cancer chemoprevention effects of Se. These results suggest that MeSeCys is converted to methylselenol more efficiently than is SeMet and that urinary TMSe and exhaled DMSe might be useful biomarkers for the generation of cancer chemopreventive forms of Se.

This study was conducted to investigate the effects of dietary selenomethionine (Se-Met) supplementation on growth performance, meat quality and antioxidant property in male broilers. A total of 800 43-day-old Lingnan yellow male broilers were randomly allotted to 5 dietary treatments with four replicates of 40 birds for a period of 3 weeks ad libitum. Final BW and weight gain of birds significantly increased by Se-Met supplementation at the 0.225 mg/kg level (P < 0.05). The addition of Se-Met significantly decreased drip loss, lightness value, and elevated pH value of meat (p < 0.05). Adding sodium selenite (SS) only increased pH value of meat (p < 0.05). In plasma, supplemental Se-Met at 0.225 mg/kg level increased total antioxidant capability (T-AOC), glutathione peroxidase (GPX), total superoxide dismutase (T-SOD), catalase (CAT) activities, glutathione (GSH) concentration (p < 0.05), and decreased malondialdehyde production (p < 0.05), compared with the control and broilers fed SS diet. In breast muscle, the addition of Se-Met significantly elevated T-AOC, GPX, T-SOD, CAT activities, contents of metallothionein and GSH (p < 0.05), and reduced carbonyl protein content (p < 0.05). While compared with broilers fed SS diet, supplemental 0.225 mg/kg Se-Met increased T-AOC, GPX, CAT activities, and GSH content (p < 0.05). Therefore, dietary Se-Met supplementation could improve growth performance and meat quality by enhancing antioxidative capacity in broilers compared with SS.

Since in the aged heart an increased basal production of reactive oxygen species (ROS) has been demonstrated, and the resistance to ROS attack could be ameliorated by antioxidant supplementation, we verified the protective effect of selenium, as sodium selenite (SS) or seleno methionine (SM), in cultured rat cardiomyocytes aged in vitro. In normoxia, glutathione peroxidase (GPx) activity and total antioxidant activity were higher in old than in young cardiomyocytes, suggesting the existence of a compensatory increase of antioxidant defenses. When aged cells were submitted to hypoxia/reoxygenation, GPx activity was not modified; while total antioxidant activity decreased, conjugated diene level increased. Selenium supplementation, particularly as SM, was able to increase GPx, and consequently total antioxidant activity, and to decrease conjugated diene production. The observed ability of selenium supplementation to protect aged cardiomyocytes from hypoxia/reoxygenation damage underlines the importance of an optimal selenium dietary intake, particularly in the elderly.

The possibility of enhancing glutathione peroxidase (GPx) activity and cytosolic total antioxidant activity (TAA) in normoxia and hypoxia/reoxygenation (H/R) by the supplementation of different concentrations of sodium selenite (SS) or selenomethionine (SM) was investigated in cultured rat cardiomyocytes. To assess the entity of oxidative stress due to H/R, levels of conjugated dienes containing lipids were determined. In normoxia, GPx activity and TAA increased in parallel with the increase in SS and SM supplementation. H/R did not influence GPx activity but lowered TAA; both SS and SM supplementations were effective in increasing GPx activity, the most effective concentration being 1 microM. At this SS and SM concentration, TAA returned to a normoxic value. Conjugated diene production, increased by H/R, was reduced by SS and SM supplementation, the 1 microM concentration appearing to be the most effective one. According to these data Se supplementation represents another possibility to counteract oxidative damage in the myocardium.