The molecular evaluation of thioredoxin (TXN1 & TXN2), thioredoxin reductase 1 (TXNRd1), and oxidative stress markers in a binary rat model of hypo- and hyperthyroidism after treatment with gallic acid.

Oxidative stress plays an important role in the pathology of thyroid disorders. This study examined the effect of gallic acid (GA) on the oxidative status and expression of liver antioxidant genes including thioredoxin (TXN1 & TXN2) and thioredoxin reductase1 (TXNRd1) in hypo- and hyperthyroid rat models. Forty-nine male Wistar rats were randomly assigned into seven groups as follows: control group, hypothyroid and hyperthyroid groups respectively induced by propylthiouracil and levothyroxine, hypo- and hyper thyroid-treated groups (where the groups were separately treated with 50 and 100 mg/kg of GA daily, orally). The levels of thyroid hormones and serum oxidative stress markers were evaluated after 5 weeks. The relative expression of TXN1,2 and TXNRd1 genes was measured via real-time qRT-PCR. The mean level of total antioxidant capacity (TAC), malondialdehyde, and uric acid index diminished in the hypothyroid group. Increased TAC reached almost the level of control in hypothyroid groups treated with GA. Elevation of thiol index in the hypothyroid group was observed (p < 0.01), which diminished to the control level after GA treatment. The relative expression of TXN1, TXNRd1, and TXN2 genes in the hypothyroid and hyperthyroid groups significantly increased compared to the control group (p ≥ 0.05), but in the groups treated with GA, the expression of these genes declined significantly (p ≥ 0.05). Our results indicated GA can affect the expression of TXN system genes in the rat liver. Also, the results suggest GA has a more positive effect on modulating serum oxidative parameters in hypothyroid rat models than in hyperthyroid.

Changes in proteins within germinating seeds of transgenic wheat with an antisense construct directed against the thioredoxin.

Thioredoxin h is closely related to germination of cereal seeds. The mechanism of transgenic wheat seeds with antisense trxs gene, which is responsible for low germination rate was studied through analyzing the changes in proteins of wheat seeds during germination. The antisense trxs could weaken the metabolism of wheat seeds by decreasing the quantity of proteins involved in metabolism, while chloroform-methanol (CM) protein fraction consisted mostly of some low molecular weight proteins (<20 kD). Compared with wild-type wheat seeds, the folding of glutenin in transgenic wheat ones was affected during the wheat maturating. Big glutenin macropolymers could be formed more easily in transgenic wheat seeds than in wild-type wheat ones. Therefore, the degradation speed of glutenin in transgenic wheat seeds was slower than that in wild-type wheat ones during seed germination. In addition, the degradation of some proteins in transgenic wheat embryos was also delayed during germination.