Gstt1, glutathione S-transferase theta 1, encodes an enzyme responsible for the detoxification of potentially harmful substances such as air pollution, drugs, pesticides, and tobacco [2]. It plays a role in protecting cells from oxidative stress by being part of the glutathione S-transferases enzyme group [1].

A meta-analysis indicated that GSTT1 polymorphisms may not be correlated with pre-eclampsia risk [1]. However, GSTT1 homozygous deletion was associated with a higher susceptibility to pancreatic cancer [3]. Also, in Caucasians, the GSTT1 null genotype was associated with prostate cancer risk [4]. Simultaneous deletion of Gstm1 and Gstt1 in CBA/CaJ mice led to more profound hearing loss under cisplatin treatment, suggesting Gstt1 protects auditory hair cells from cisplatin-induced ototoxicity [5]. GSTT1-null genotype was associated with increased bladder cancer risk in Caucasians [6]. The frequency of Gstt1 in gallbladder cancer patients was high before treatment but decreased after treatment [7]. In solid organ and hematopoietic stem cell transplantation, GSTT1 donor-recipient mismatch is associated with immune-related issues [8]. The GSTT1 null genotype was associated with increased coronary heart disease risk, and there was a positive interaction between the GSTT1 null genotype and smoking status [9]. In Asians, the GSTT1 null genotype was associated with increased lung cancer risk, especially in the Chinese population [10].

In conclusion, Gstt1 is crucial for detoxification and protecting cells from oxidative stress. Studies using gene-deletion models, such as the simultaneous deletion of Gstm1 and Gstt1 in mice, have revealed its role in various disease conditions including cancer, pre-eclampsia, cisplatin-induced ototoxicity, and coronary heart disease. These findings contribute to understanding disease mechanisms and may guide future research in disease treatment and prevention.