Changes in the oxidative stress factors and inflammatory proteins following the treatment of BPH‐induced dogs with an anti‐proliferative agent called tadalafil

Abstract

Background Finding a medical treatment which can combat cell proliferation and relax smooth muscles in canine benign prostatic hyperplasia (BPH) appears to be imperative. Aims This study aimed to evaluate the oxidative stress and inflammatory proteins following the treatment of dogs induced for BPH with an anti‐proliferative agent called tadalafil. Materials and Methods Twenty‐five adult intact male dogs were randomly designated into five groups (n = 5): Control group was not induced for BPH and not treated with tadalafil; dogs induced for BPH by testosterone enanthate and estradiol benzoate and treated with tadalafil (5 mg/day P.O.); dogs which received tadalafil (5 mg/day P.O.); dogs induced for BPH and treated with castration; and dogs induced for BPH. Oxidative stress factors (glutathione peroxidase [GPX], superoxide dismutase [SOD], catalase) and inflammatory proteins (haptoglobin, serum amyloid A [SAA], malondialdehyde [MDA]) were measured in the blood serum for four sequential weeks. Results Glutathione peroxidase and SOD serum levels declined in dogs in the BPH‐induced group compared to those in the control group. Those levels diminished in BPH‐induced castrated and tadalafil‐treated groups. The changes in the GPX and SOD serum concentrations were not significant between the BPH‐induced castrated group and BPH‐induced tadalafil‐treated group. Moreover, MDA concentration increased slightly in groups with BPH and groups which were castrated. Generally, however, there were no significant differences in the MDA serum concentrations between other groups. Haptoglobin and SAA concentrations increased in BPH‐castrated group. Also, the differences in haptoglobin and SAA were not significant between the groups. Conclusion Tadalafil could not control oxidative stress and inflammatory mediators which happened during BPH in dogs.

Reproductive and endocrinological effects of Benign Prostatic Hyperplasia and finasteride therapy in dogs

“…The excessive production of reactive oxygen species (ROS), changes in pH and osmolarity of the seminal fluid are common causes of premature hyperactivation 32 . However, oxidative stress and ROS generation are considered to occur only in severe and chronic prostatic disorders, with loss of prostatic parenchyma integrity 11 , 15 . In fact, we could not find significant differences in oxidative stress (TBARS) and antioxidant activity (SOD and GPx) within experimental groups.…”

“…The lack of endocrine equilibrium leads to a quantitative increase in prostate androgen receptors, upregulating testosterone action 5 , 9 , which is the pivotal reason for a markedly conversion of testosterone into dihydrotestosterone (DHT) by the enzymatic action of 5α-reductase 7 , 9 . Increased DHT concentrations provoke several prostatic alterations, such as hypertrophy and hyperplasia of glandular cells, angiogenesis 9 and even local oxidative stress in men 10 and dogs 11 .…”

Changes in specific serum biomarkers during the induction of prostatic hyperplasia in dogs

“…They were treated with antiparasitic drugs (one tablet of praziquantel for 10 kg/BW and one tablet of mebendazole for 5 kg/BW) for 2 weeks. All dogs were fed 300 g of commercial dog food (NUTRI® Dry Dog Food; Behintash Co. Iran) daily [38,39]. The volume of each prostate was determined by ultrasonography examination.…”

“…In the PH induction group, dogs received testosterone enanthate (Caspian Tamin, Iran; 75 mg/dog) and estradiol benzoate (Aburaihan, Iran; 0.75 mg/dog) via intramuscular injection on days 0, 21, 42, and 63. The testosterone doses were doubled on days 21 and 42 [38,39,42]. Blood sampling was performed from the jugular vein into glass tubes.…”

Can Botulinum Toxin A Still Have a Role in Treatment of Lower Urinary Tract Symptoms/Benign Prostatic Hyperplasia Through Inhibition of Chronic Prostatic Inflammation?

“…Elderly patients with LUTS showed decreased prostate perfusion on transrectal color Doppler ultrasonography [7]. Serum glutathione peroxidase and superoxide dismutase levels, which have antioxidant effects, reportedly declined in dogs with BPH [65]. Oxidative stress also triggers prostate cells proliferation through the activation of cyclooxygenase (COX) pathways [66,67], whereas COX-2 inhibition can induce significant apoptosis in the prostate cell [67].…”