Biochemical and oxidative stress markers in the liver and kidneys of rats submitted to different protocols of anabolic steroids

Abstract

The objective of this study was to evaluate the effects of different protocols (P1, P2, and P3) of boldenone undecylenate (BU) and stanozolol (ST) on markers of liver and kidney function and variables of oxidative stress in these organs. For this, 54 male Wistar rats were divided into nine groups of six animals each. Each animal received intramuscularly 5.0 mg kg of BU or ST once a week for 4 weeks (P1); 2.5 mg kg of BU or ST once a week for 8 weeks (P2); and 1.25 mg kg of BU or ST once a week for 12 weeks (P3). For each protocol, a control group was used, and they received 0.1 ml of olive oil intramuscularly. Blood and fragments of liver and kidney were collected for alanine aminotransferase activity (ALT), alkaline phosphatase, albumin, creatinine, cholesterol, total protein, triglycerides, urea, reactive oxygen species, thiobarbituric acid reactive substances, total thiols, and glutathione evaluation. The results show that the BU in doses of 5 (day 30) and 2.5 mg kg (day 60) changes the ALT seric activity, possibly showing a hepatotoxic effect. High doses of BU may lead to increased levels of cholesterol (protocol P1) possibly due to inhibition of the normal steroid biosynthesis process. All protocols used caused changes in the redox balance of the organs studied (except in the liver, protocol P2), which indicates that these drugs might be harmful even at low doses.

Antioxidant, hepatoprotective, genoprotective, and cytoprotective effects of quercetin in a murine model of arthritis

“…Production of ROS occurs in every cell type, and these molecules can affect various cellular functions including cell signaling, angiogenesis, apoptosis, and cell proliferation . The damaged caused by ROS to lipids and other biological molecules results in unstable and highly reactive lipid hydroperoxides, whose break down generates thiobarbituric acid‐reactive substances (TBARS) …”

“…6 Production of ROS occurs in every cell type, and these molecules can affect various cellular functions including cell signaling, angiogenesis, apoptosis, and cell proliferation. [7][8][9] The damaged caused by ROS to lipids and other biological molecules results in unstable and highly reactive lipid hydroperoxides, whose break down generates thiobarbituric acid-reactive substances (TBARS). [10][11][12] Besides, DNA damage caused by ROS can include genome instability, increased mutation, apoptosis, and associated tissue regeneration and cell proliferation.…”

Stanozolol promotes lipid deposition in the aorta through an imbalance in inflammatory cytokines and oxidative status in LDLr knockout mice fed a normal diet

“…However, the literature regarding these effects seems inconsistent since there are also reports that show reduction and no changes in the lipid profiles after the use of steroids . However, this effect seems to depend on dose, time and the type of AAS used, and it is necessary to clarify the impacts of these factors on the development of atherosclerosis, which is an important risk factor for the development of cardiovascular diseases described in animals and human beings …”

“…Stanozolol is a non‐aromatizable steroid derived from dihydrotestosterone and is one of the most used steroids worldwide . The use of stanozolol at high doses and for a prolonged time can trigger a wide variety of adverse effects, which are still not well described in the literature …”

“…The evidence shows that stanozolol is capable of increasing the concentrations of low‐density lipoprotein cholesterol (LDL‐C), stimulating the immune response and promoting oxidative stress . All of these processes are crucial for the development of atherosclerosis .…”