Gstt1, glutathione S-transferase theta 1, encodes an enzyme responsible for the detoxification of substances potentially harmful to the human body, such as air pollution, drugs, pesticides, and tobacco [2]. The enzyme is part of the glutathione S-transferases (GST) group that protects cells from oxidative stress [1].

Some studies suggest associations between Gstt1 polymorphisms and various diseases. A meta-analysis indicated that Gstt1 homozygous deletion may increase susceptibility to pancreatic cancer [3]. In prostate cancer, the Gstt1 null genotype was associated with risk in Caucasians [4]. Gstt1 null, along with Gstm1 null, was associated with increased bladder cancer risk in Caucasians [6]. Also, in coronary heart disease, the Gstt1 null genotype was associated with increased risk, and there was a positive interaction with smoking status [7]. In lung cancer, the Gstt1 null genotype was associated with increased risk in Asians, especially in Chinese populations [8]. In CBA/CaJ mice, simultaneous deletion of Gstm1 and Gstt1 led to more profound hearing loss under cisplatin treatment, suggesting Gstt1 protects auditory hair cells from cisplatin-induced ototoxicity [5].

In conclusion, Gstt1 plays a crucial role in detoxification and protection against oxidative stress. Studies using genetic models, such as gene deletions in mice, have revealed its significance in various disease conditions including cancer, heart disease, and ototoxicity. Understanding Gstt1's function through these models provides insights into disease mechanisms and potential preventive or treatment strategies.