Some neurologic, cardiovascular, and cancer diseases have been associated with alterations in serum lipid profiles [10, 23, 24]. The results of a study by Gibanananda Ray et al. [24], which investigated the role of lipids and lipoproteins in breast cancer patients, showed that high levels of TG may play a significant role in developing cancer. In addition, plasma LDL concentrations increase, which is more prone to oxidation and may lead to higher lipid peroxidation in cancer patients. In this study, HDL concentrations were reduced and may not adequately counteract the high ROS production. It has been reported that free radicals initially cause oxidative stress in breast cancer patients and lead to cell proliferation and malignant transformation [24]. In a study of cervical cancer patients, TG was higher in the patients than in the control group and was statistically significant. There was a significant decrease in serum HDL. TG is a consequence of cervical cancer, and as cancer progresses from stage 1 to stage 4, chol and LDL increase [25].
In a study by Abas AM et al. [26], cancer patients were found to have elevated plasma LDL concentrations, which are more sensitive to oxidation and may lead to higher lipid peroxidation in breast cancer patients and oxidative stress. This study is associated with lymph node metastases in men with colorectal carcinoma, LDL levels increase, and HDL levels decrease. Decreased HDL levels in premenopausal women may be a marker of increased breast cancer risk [26]. However, in this study, as in our study, TG levels did not differ significantly between the healthy and control groups. In our study, serum levels of TG, LDL, and cholesterol were higher in the patients than in the healthy group. However, statistically, no significant increase in their serum levels was observed. The serum level of HDL was also lower in the patient group than in the healthy group. However, this was not statistically significant. These changes may be due to people's diets or lifestyles.
According to the results of our study, the mean serum level of SOD and MDA was higher in the patient group than in the control group; this increase was statistically significant. However, the mean serum level of Gpx and CAT in the patient group was increased compared to the control group, but this increase was not statistically significant. The mean TAC level was lower in the patient group than in the control group, which was not statistically significant and caused high toxicity and inhibition of protective enzymes, so MDA is approved as a mediator of tumor promotion and carcinogenesis [27]. Increased MDA levels and oxidative stress index are associated with a disturbed balance between oxidants and antioxidants, and these findings are supported by a decrease in antioxidant capacity [28]. The increase in MDA in cancer patients is due to the oxidation of membrane fatty acids stimulated by free radicals [29]. A study of patients with breast and cervical cancer found that lipid peroxidation increased in these patients, and MDA levels showed a statistically significant increase [30]. In Iraq, another 2011 study by Razooki et al. examined changes in lipid peroxidation and concentrations of certain elements in the serum and tissues of patients with uterine cancer. It concluded that MDA levels were significantly higher in patients than in the control group. This increase was also significantly increased in women close to menopause compared with other groups [31]. The mean serum level of MDA was higher than expected in the patient group due to increased lipid peroxidation in patients. The probable reason for the high lipid peroxidation level in cancer is decreased antioxidant capacity.
Low TAC levels may indicate oxidative stress or increased susceptibility to oxidative damage [8]. A study by Zińczuk et al. on colorectal cancer patients found that plasma TAC levels were significantly lower in cancer patients than in control subjects. In this study, it was reported that increased ROS formation or inadequate elimination leads to cancer. The results of this study support the increase in oxidative stress and the decrease in antioxidant defense in breast cancer patients [32]. In agreement with our study, Mahmood et al. investigated breast cancer patients. It was found that serum TAC levels were lower in breast cancer patients than in healthy women. These results may indicate increased oxidative stress in patients and a depletion of the body's antioxidant capacity [33]. Our results follow most previous findings suggesting that the increase in ROS may be due to decreased levels of antioxidants in the body, which significantly increases lipid peroxidation in serum.
A group in India studied lipid peroxidation, antioxidants, and red blood cell osmotic fragility in the blood of patients with cervical cancer. They found an increase in lipid peroxidation, insufficient levels of antioxidants, and an alteration in the ratio of cholesterol to phospholipids in the membrane of red blood cells. In addition, they discovered abnormalities in the structure, functioning, and operation of the Na-K-ATP-Ase pump. They examined the activity of SOD, CAT, and Gpx in patients and reported a decrease in SOD and an increase in CAT and Gpx [34]. One study investigated the expression of antioxidant enzymes in patients with uterine polyps, fibroids, hyperplasia, and adenocarcinoma. The results showed a decrease in SOD, CAT, and Nrf2 and increased GPx and glutathione reductase (GR) levels in hyperplasia. In patients with adenocarcinoma, the levels of CAT decreased, and GR increased compared with the benign groups [35]. To measure oxidative stress in the blood, a team examined lipid peroxidation levels and enzymatic antioxidant status in women with uterine conditions, including uterine tumors, endometrial polyps, and malignant endometrium.
The results showed that changes in measured parameters differed according to the statute of enzyme and the type of disease diagnosed. Disturbances of antioxidants in the blood of patients with malignant endometrium are more pronounced than in other diseases. Although the activity of SOD was lower in the blood of the patient group, the decrease in activity was greater in patients with hyperplasia and adenocarcinoma than in patients with polyps or fibroids. The decrease in SOD activity may be due to increased androgenic ROS production by lipid peroxidation. Lipid hydroperoxide levels are negatively correlated with SOD and Gpx and positively correlated with catalase. The ratio of lipid hydroperoxides to GPx also increased according to the statute of uterine disease. A significant increase in CAT activity was observed only in patients with hyperplasia. There was a significant increase in GPx activity in patients with polyps, whereas its activity decreased in the other groups [36]. The mean serum level of SOD was increased in the group of uterine cancer patients. Since cancer and oxidative stress are related, it was expected that the serum level of this antioxidant would decrease. However, based on previous studies and the direct effect of various factors such as cancer type, disease stage, monopoiesis status, and using various drugs on the changes in antioxidant status, this increase can be justified.