Breast cancer is one of the most common malignancies in women and the leading cause of cancer mortality. Hypercholesterolemia and obesity are potential risk factors for the incidence of breast cancer, and their detection can enhance cancer prevention. In this paper, we discuss the current state of investigations on the importance of lipoproteins, such as low denisity lipoproteins (LDL) and high density lipoproteins (HDL), and cholesterol transporters in the progression of breast cancer, and the therapeutic strategies to reduce breast cancer mortality. Although some research has been unsuccessful at uncovering links between the roles of lipoproteins and breast cancer risk, major scientific trials have found a straight link between LDL levels and incidence of breast cancer, and an inverse link was found between HDL and breast cancer development. Cholesterol and its transporters were shown to have significant importance in the development of breast cancer in studies on breast cancer cell lines and experimental mice models. Instead of cholesterol, 27-hydroxycholesterol, which is a cholesterol metabolite, is thought to promote propagation and metastasis of estrogen receptor-positive breast cancer cell lines. Alteration of lipoproteins via oxidation and HDL glycation are thought to activate many pathways associated with inflammation, thereby promoting cellular proliferation and migration, leading to metastasis while suppressing apoptosis. Medications that lower cholesterol levels and apolipoprotein A-I mimics have appeared to be possible therapeutic agents for preventing excessive cholesterol’s role in promoting the development of breast cancer.

Iron is a crucial element required for the proper functioning of the body. For instance, hemoglobin is the vital component in the blood that delivers oxygen to various parts of the body. The heme protein present in hemoglobin comprises iron in the form of a ferrous state which regulates oxygen delivery. Excess iron in the body is stored as ferritin and would be utilized under iron-deficient conditions. Surprisingly, cancer cells as well as cancer stem cells have elevated ferritin levels suggesting that iron plays a vital role in protecting these cells. However, apart from the cytoprotective role iron also has the potential to induce cell death via ferroptosis which is a non-apoptotic cell death dependent on iron reserves. Apoptosis a caspase-dependent cell death mechanism is effective on cancer cells however little is known about its impact on cancer stem cell death. This paper focuses on the molecular characteristics of apoptosis and ferroptosis and the importance of switching to ferroptosis to target cancer stem cells death thereby preventing cancer relapse. To the best of our knowledge, this is the first review to demonstrate the importance of intracellular iron in regulating the switching of tumor cells and therapy resistant CSCs from apoptosis to ferroptosis.

The effect of selected pesticides, monocrotophos, chlorpyrifos alone and in combination with mancozeb and carbendazim, respectively, was tested on nitrification and phosphatase activity in two groundnut (Arachis hypogeae L.) soils. The oxidation of ammonical nitrogen was significantly enhanced under the impact of selected pesticides alone and in combinations at 2.5 kg ha(-1) in black soil, and furthermore, increase in concentration of pesticides decreased the rate of nitrification, whereas in the case of red soil, the nitrification was increased up to 5.0 kg ha(-1) after 4 weeks, and then decline phase was started gradually from 6 to 8 weeks of incubation. The activity of phosphatase was increased in soils, which received the monocrotophos alone and in combination with mancozeb up to 2.5 and 5.0 kg ha(-1), whereas the application of chlorpyrifos singly and in combination with carbendazim at 2.5 kg ha(-1) profoundly increased the phosphatase activity after 20 days of incubation, in both soils. But higher concentrations of pesticides were either innocuous or inhibitory to the phosphatase activity.

Introduction of agrochemicals (fungicides) into soil may have lasting effects on soil microbial activities and thus affect soil health. In order to determine the changes in microbial activity in a black clay and red sandy loam soils of groundnut (Arachis hypogaea L.) cultivated fields, a case study was conducted with propiconazole and chlorothalonil to evaluate its effects on soil enzymes (cellulase and invertase) throughout 40 days of incubation under laboratory conditions with different concentrations (1.0, 2.5, 5.0, 7.5, and 10.0 kg ha−1). Individual application of the two fungicides at 1.0, 2.5, and 5.0 kg ha−1 to the soil distinctly enhanced the activities of cellulase and invertase but at higher concentrations of 7.5 and 10 kg ha−1 was toxic or innocuous to both cellulase and invertase activities. In soil samples receiving 2.5–5.0 kg ha−1 of the fungicides, the accumulation of reducing sugar was pronounced more at 20 days, and the activity of the cellulase and invertase was drastically decreased with increasing period of incubation up to 30 and 40 days.

In practice pesticides are extensively used in agriculture as a part of pest control strategies. Two insecticides, endosulfan (organochlorine) and profenophos (organophosphate), were assessed for their effects on the activities of protease (in terms of tyrosine formed from casein) and urease (as ammonia released from urea) in soil, collected from a fallow groundnut field by applications of insecticides at normal field rates and at higher concentrations (1.0, 2.5, 5.0, 7.5, 10.0 kg ha -1 ), in a laboratory study. The results showed a strong positive influence on protease and urease enzyme activities in soil treated with 2.5 and 5.0 kg ha -1 dry soil and they were significantly (P ≤ 0.05) higher than the control over the course of incubation. In soil treatment, there was a significant increase in protease and decrease in urease activities after 24h of incubation which continued up to 20 days. However, a significant decrease in both protease and urease enzyme activities was observed in 30 and 40 days of incubation.