shed light on this putative relationship [ 94 ]. It is worth noting that a reduction in total glutathione implies a problem with synthesis of glutathione, whereas a decrease in GSH implies an anomaly in GSH:GSSG. Both have been observed in autism spectrum disorders [ 46 - 48 , 50 , 77 , 81 , 82 , 85 , 87 , 91 ]. As the bioavailability of cysteine is the rate limiting factor for synthesis of GSH [ 31 - 34 ], the lower cysteine levels detected in serum of children with autistic disorder could be an important factor leading to the lower levels of GSH observed in many children with this condition [ 46 - 48 , 50 , 81 , 82 ]. While several studies examined GPx activity [ 63 , 71 , 72 , 74 , 81 , 83 , 84 ] or its polymorphisms [ 94 , 95 ], only one examined glutathione reductase or glutathione-S-transferase activity [ 85 ]. The higher level of GSSG observed in the serum of many children with autism spectrum disorders [ 46 - 48 , 50 , 85 , 87 , 91 ] is likely to truly reflect increased oxidative stress as there is no significant difference in GPx-1 activity in serum or platelets [ 63 , 84 ] and GPx-1 is significantly lower in the erythrocytes of children with autistic disorder compared to controls. As cysteine itself may have strong anti-oxidant properties, its lower concentration in children with autistic