Effects of selenocystine on lead-exposed Chinese hamster ovary (CHO) and PC-12 cells

Abstract

Lead is a pervasive environmental toxin that affects multiple organ systems, including the nervous, renal, reproductive, and hematological systems. Even though it is probably the most studied toxic metal, some of the symptoms of lead toxicity still cannot be explained by known molecular mechanisms. Therefore, lead-induced oxidative stress has recently started to gain attention. This in vitro study confirms the existence of oxidative stress due to lead exposure. Administration of lead acetate (PbA) to cultures of Chinese hamster ovary cells (CHO) had a concentrationdependent inhibitory effect on colony formation and cell proliferation. This inhibition was eliminated by 5 μM selenocystine (SeCys). In order to evaluate the nature of SeCys's effect, we measured glutathione (GSH), its oxidized form glutathione disulfide (GSSG), malondialdehyde (MDA), catalase, and GSH peroxidase (GPx) activities in lead-exposed CHO cells both in the presence and absence of SeCys. Increases in MDA, catalase, and GPx activities were observed in cultures that received only PbA, but supplementation with SeCys returned these measures to pretreatment levels. The ratio of GSH to GSSG increased in lead-exposed cells incubated in SeCys-enhanced media but declined in cultures treated with PbA only. In order to determine whether SeCys also reverses lead-induced neurotoxicity, a neuronal cell line, PC-12 cells, was used. Lead's inhibition on neurite formation was significantly eliminated by SeCys in PC-12 cells. Our results suggest that SeCys can confer protection against leadinduced toxicity in CHO cells and neurotoxicity in PC-12 cells.

The Role of the Antioxidant Enzymes in Erythrocytes in the Development of Arterial Hypertension among Humans Exposed to Lead

“…Some clinical studies confirm the activation of antioxidants as a result of lead action [13,20]. Also, in vitro administration of lead acetate (500 μmol/l) to cell cultures showed an increase of both MDA concentration and antioxidant enzymes activity (GPx, CAT) [21]. On the other hand, the incubation of erythrocytes in the presence of lead (5 μmol/l) inhibited the activity of GPx, SOD, and catalase [22].…”

Protective Effects of Selol Against Sodium Nitroprusside-Induced Cell Death and Oxidative Stress in PC12 Cells

“…We showed that the protective mechanism of Selol against SNP cytotoxicity included significant inhibition of ROS production along with the restoration of GSH homeostasis, and the expression/activity of antioxidative enzymes. Similarly, Aykin-Burns et al showed that selenocystine (SeCys) also ameliorated lead-induced imbalance of the GSH/GSSG ratio [55]. In addition, pretreatment with SeMet for 16 h has been shown to protect primary rat hippocampal neurons against the toxicity of ROS generated by iron/hydrogen peroxide (Fe 2+ /H 2 O 2 ) or amyloid β.…”

Oxidative stress‐alleviating strategies to improve recombinant protein production in CHO cells

“…Moreover, the medium composition has to be considered when supplementing cultures with selenium as this compound can interact with other trace elements. Finally, selenocysteine supplementation has also been demonstrated to decrease cell death of CHO cells exposed to lead‐induced oxidative stress (Aykin‐Burns & Ercal, ).…”

“…Finally, selenocysteine supplementation has also been demonstrated to decrease cell death of CHO cells exposed to lead-induced oxidative stress (Aykin-Burns & Ercal, 2006).…”