Cancer is the world's second-greatest cause of mortality, accounting for 9.6 million fatalities in 2018. Individual and environmental traits, lifestyle, and genetics are all risk factors for cancer [1]. Breast cancer is a widespread disease among women, with one million new patients diagnosed each year and 400,000 fatalities [2]. Although ovarian cancer (OC) is the seventh most commonly diagnosed form of cancer in women around the world, the risk of developing ovarian cancer is higher for women who have ovulated more frequently during their lifetimes. [3]. Changes in inflammatory state, genetic modifications, ionizing radiation exposure, oxidative stress, and trace elements are all risk factors [1]. The metabolic redox events that occur normally during cell metabolism are the source of reactive oxygen species (ROS), which include O ^2•-, H₂O₂, and OH^•. These highly reactive species are produced by the cell. When reactive oxygen species (ROS) are unable to scavenge excess oxygen-produced free radicals, important biomolecules are destroyed. Exposure to environmental stimuli, including as ultraviolet light, cigarette smoke, environmental contaminants, and gamma radiation, promotes the creation of ROS [4-5]. Patients and doctors should stress the relevance of oxidants and antioxidants at various clinical and pathological phases of the disease.; however, nursing, tubal ligation, and hormonal birth control can reduce the risk. The aim of the present study was to determine whether an oxidative stress occurs in breast and ovary cancers.

Data Collection

A questionnaire created especially to gather data on demographics and clinical information was used to collect the data.

Subjects

Forty women with breast, ovarian cancer and twenty healthy women were involved in current study, that the samples were collected from the tumor centers in Najaf from women who suffer from the required condition.

The patients’ blood serums were carefully stored until tests were conducted on them. About 2ml of blood serum was taken from patients to test.

Assay Procedures

The estimation of serum malondialdehyde (MDA), and catalase were performed spectrophotometrically by using commercially available kit of Solarbio. The principle of tumor markers CA125 and CA3-15 CA 125 is done by using one -step sandwich assay).

Statistical Analysis

The data were reported using means and standard deviations. The method was utilised to carry out the statistical analyses. ANOVA followed by LSD test for multiple comparisons by using SPSS version 20 computer program. The P ≤ 0.05 were considered a significant for all data of the results.

In this study, the mean age of patients with breast cancer is (53±8.1), ovary (44±6.2) years and the mean age of control group is (45±14.6) years. There were no smokers in all groups and none of the patients were suffering from diabetes and no patients seem to be taking any antihypertensive drugs as shown in Table 1. 

Table 1: Clinical Characteristics of the Patients

However, the results show that 25% of ovary patients didn’t have medicine, 57% of healthy women didn’t take any medicine while breast patients have been taking medicine (100%) of breast patients had chemotherapy while (50%) of ovary patients had chemotherapy and none of control had chemotherapy.

The MDA-reactive product estimates for the cancer patients and controls are provided in Table (2). 

Table 2: Comparison of Mda Among Breast C. Ovary C. and Controls

The mean 6.765± 0.87 mmol/l vs. 4.804 ±2.048, P = 0.1067) and the MDA level between ovarian cancer patients and breast cancer patients (mean 6.765± 0.87 mmol/l vs. 9.33 ± 2.28, P = 0.0674) were not significantly different from each other. The study found that patients with breast cancer had considerably greater levels of lipid peroxidation products (mean 9.33 ± 2.28 mmol/l) compared to the healthy controls (4.804 ± 2.048 mmol/l; P = 0.0030).

The findings of catalase activity estimation in patient serum are reported in Tables 3. 

Table 3: Comparison of Catalase Among Breast C. Ovary C. and Controls

Catalase activity in ovarian cancer patients was not substantially different from that in breast cancer patients (mean 1.695±0.875 U/gHb vs1.86 ±0.885 U/gHb, p = 0.774, t.test) Catalase activity differed significantly between patients with breast cancer and controls (mean 1.86 0.885 U/gHb vs. 3.586 1.282 U/gHb, p = 0.0383, t-test). Catalase activity in ovarian cancer patients seemed to be lower than in controls, although the difference was not significant (1.695±0.875 U/gHb vs. 3.586±1.282 U/gHb, p:0.0261).

Table 4: Comparison of Serum Levels of Tumor Marker Ca 3-15

The serum levels of CA125 and CA3-15 in the malignant groups were considerably higher than in the control and benign groups, as indicated in tables 4 and 5.

Table 5 comparison of serum levels of tumor marker Ca 125

The human body's antioxidative defence systems may be subjected to an oxidative load caused by malignant tumours [6]. Previous studies indicated that patients with cancer had reduced levels of the antioxidant enzymes Cu/Zn-SOD, CAT, and GPX. The vast majority of these studies have focussed their attention on the levels of antioxidant enzyme expression that can be identified using immunohistochemistry in tumour tissues [7].

The levels of antioxidant enzyme activity and MDA levels in the blood, which are regarded as criteria for the overall oxidative status of the human organism, have only been documented in a select few articles. When Boyd and McGuire looked at the levels of MDA in the urine of 30 breast cancer patients, they found that it was twice as high as the levels in the urine of healthy controls [8].

According to the findings presented here, women who had malignant tumours in their bodies prior to receiving any treatment had a higher plasma production of lipid peroxidation products than the controls did. After this, there is a decrease in the activity of CAT, which is an antioxidant defence enzyme. It's possible that the higher MDA levels in cancer patients are the result of still-active environmental and drug risk factors, in addition to a main or secondary disruption in the antioxidant enzyme system. It is possible that monocytes, during the process of phagocytosing tumour cells [9] and cancer tissues [10], are significant causes of increased ROS formation. The levels of MDA in people who had advanced cancer were surprisingly lower than those in persons who had early-stage cancer. In the screening process for gynecologically malignant pelvic tumours, CA125 is a marker that is frequently employed. In order to generate response material, tumour markers are created in the tumour cells of the host; however, under normal circumstances, only a trace amount is seen in the serum. Its expression increases along with the progression of the tumour, and it is highly expressed in epithelial ovarian tumour cells as well as in serous ovarian adenocarcinoma. CA15-3 is a glycoprotein that is a member of the mucin-1 (MUC-1) family. It is overexpressed in malignancies, and it has been discovered as a possible tumour marker [11]. This is because aberrant glycosylation causes CA15-3 to be overexpressed. Carcinoembryonic antigen, or CEA, is a type of cell adhesion molecule. Research has shown that elevated blood levels of CEA are associated with tumour metastasis [12–13]. 

The findings of current study imply that oxidative stress is elevated in cancer patients (breast and ovarian cancer), as seen by increased MDA and decreased catalase serum levels.

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