Our objective was to assess the pattern of type-2 diabetes-associated androgen alteration in patients with erectile dysfunction (ED). A total of 127 diabetic male patients with ED were enrolled in this study. Erectile function was assessed using the International Index of Erectile Function (IIEF). At the time of assessment, patients were also interviewed and assessed for socio-demographic and medical history that includes duration and severity of diabetes mellitus (DM). Patients underwent routine laboratory investigations, in addition to total testosterone (T), dehydroepiandrosterone sulphate (DHEA-S) and insulin assessment. The mean age +/- SD was 53.8 +/- 9.3 years. Of patients 25.2% (n = 32/127), 6.3% (n = 8/127) and 31.5% (n = 40/127) had low total T, low DHEA-S and hyperinsulinaemia respectively. There were significant association between the increase in age and body mass index and the presence of low T level. Of the patients 37.5% (n = 12/32) with low T level had glycosylated haemoglobin (HbA1c) >7% while, 22.1% (n = 21/95) of the patients with normal T level had HbA1c >7% (p < 0.05). There were significant associations between the number of patients with low level of total T or DHEA-S and poor control of DM. Patients with low T level were two times more likely (56.3%, n = 18/32) to have severe ED than patients with normal T level (27.4%, n = 26/95) (p < 0.01). There were significant differences between the mean levels of total T or DHEA-S and poor control of DM. No significant associations were detected between hyperinsulinaemia and the level of fasting blood sugar, duration of DM, metabolic control of DM or ED severity. Patients with low T level were three times as likely to have hyperinsulinaemia as those patients with normal T level (p < 0.05). The current study clearly demonstrated that there were significant associations between low level of total T or DHEA-S and poor control of DM.

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Doxorubicin (DOX), an anthracycline antibiotic, is an important antineoplastic agent due to its high antitumor efficacy in hematological as well as in solid malignancies. The clinical use of DOX is limited due to its cardiotoxic effects. The present study aimed to investigate the possible protective effect of olmesartan (Olm), l-carnitine (L-CA), and their combination in cardiotoxicity induced by DOX in rats. Male albino rats were randomly divided into seven experimental groups (n = 8): group I: normal control, group II: L-CA, group III: Olm, group IV: DOX. The other three groups were treated with Olm (10 mg/kg), L-CA (300 mg/kg), and their combination for 2 weeks after induction of cardiotoxicity by a single dose of DOX (20 mg/kg). In the results, DOX showed a significant elevation in serum troponin I, creatine kinase-MB (CK-MB), and lactate dehydrogenase (LDH) together with increased inflammation manifested by the rise of tumor necrosis factor-alpha (TNF-α), intercellular adhesion molecules-1 (ICAM-1), interleukin IL-1β (IL-1β), myeloperoxidase (MPO), nuclear factor-kappa B (NF-κB), and transforming growth factor beta (TGF-β) in cardiac tissues as well as DOX-induced oxidative stress by increasing in malondialdehyde (MDA) and decreasing in superoxide dismutase (SOD) and glutathione (GSH) in heart tissues. In addition, caspase-3 activity was boosted as indication of increased apoptosis. On the other hand, administration of L-CA and Olm attenuated the DOX-evoked disturbances in the abovementioned parameters. In addition, DOX exhibited echocardiographic changes and severe histopathological changes, which were significantly reversed by L-CA and Olm treatment. In conclusion, the present study data confirm the protective role of L-CA and Olm in DOX-induced cardiotoxicity, which may be related to its antioxidant, antiinflammatory, and antiapoptotic agents.

Being one of the most abundant trace elements in the human body, the therapeutic potential of tellurium-based compounds has been a target of interest. Recent reports denoted their redox-modulating and anti-inflammatory activities in experimental endotoxemia. However, their potential nephroprotective effect against endotoxemic kidney injury is yet to be elucidated. This study investigated the possible renoprotective effect of telluric acid (TEL) against lipopolysaccharide (LPS)-induced acute kidney injury (AKI) in mice, targeting toll-like receptor 4 (TLR4), phosphoinositide 3-kinase (PI3K)/Akt, and nuclear factor-erythroid 2-related factor-2 (Nrf2) pathways as possible mechanistic contributors to TEL's effect. AKI was induced by LPS (2 mg/kg). TEL (60 μg/kg; i.p.) was administered once daily for seven consecutive days before LPS injection. Pretreatment with TEL alleviated LPS-induced AKI as evidenced by the hampered serum levels of creatinine and cystatin C. TEL also opposed LPS-induced elevation in renal kidney injury molecule-1, neutrophil gelatinase-associated lipocalin, nuclear factor-kappa B p65, interleukin-1β, and thiobarbituric acid-reactive substance contents. This was accompanied by a replenishment of renal glutathione, transcriptional upregulation of Nrf2, enhancement of heme oxygenase-1 activity, and a marked upregulation of phospho-PI3K and phospho-Akt protein expressions. Histopathological findings corroborated with the amendment of biochemical parameters. In view of these findings, we may conclude that TEL pretreatment purveyed novel nephroprotective effects against endotoxemic kidney injury, which might be partly attributed to the modulation of TLR4, PI3K/Akt, and Nrf2 signaling pathways and may hence provide a valuable asset for the management of endotoxemic renal complications.

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