Curcumin and Vitamin C Attenuate Gentamicin-Induced Nephrotoxicity by Modulating Distinctive Reactive Species.

Gentamicin remains widely used in all age groups despite its well-documented nephrotoxicity; however, no adjuvant therapies have been established to counteract this side effect. Our study aimed to experimentally determine whether curcumin and vitamin C have nephroprotective effects and whether certain reactive species could be used as markers of early gentamicin nephrotoxicity. Wistar adult male rats were evenly distributed into four groups: control, gentamicin, curcumin and gentamicin, vitamin C and gentamicin (gentamicin: 60 mg/kg/day, intraperitoneally, 7 days). We determined renal function (urea, creatinine), oxidative stress (malondialdehyde, nitric oxide, 3-nitrotyrosine, total oxidative stress), and antioxidant and anti-inflammatory status (thiols, total antioxidant capacity, interleukin-10). Nephrotoxicity was successfully induced, as shown by the elevated creatinine levels in the gentamicin group. In contrast, supplementation with curcumin and vitamin C prevented an increase in urea levels while decreasing total oxidative stress levels compared to the gentamicin group. Moreover, vitamin C and curcumin distinctively modulate the levels of nitric oxide and malondialdehyde. Histological analysis showed more discrete lesions in rats that received vitamin C compared to the curcumin group.

Accelerated lipid peroxidation in a rat model of gentamicin nephrotoxicity.

Kidney disease represents a burden for the health care system worldwide. As the prevalence continues to rise, discovering new biomarkers of early kidney damage has become crucial. Oxidative stress (OS) represents one of the main factors involved in the early stages of many syndromes leading to kidney damage. Therefore, it must be studied in detail. To date, many studies have focused on OS in advanced stages of acute kidney injury (AKI), with great success. The aim of the present study was to ascertain whether even mild renal function impairment can be linked to specific systemic markers of OS and systemic antioxidants in order to pinpoint certain biomarkers for early kidney damage. We used male rats (Rattus norvegicus) in which we induced kidney damage by injecting gentamicin for 7 days. Blood was collected 24 h after the last dose of gentamicin. Urea, creatinine, 3-nitrotyrosine (3-NT), nitric oxide (NO), malondialdehyde (MDA), thiols (TS), total oxidative stress (TOS), and interferon-γ (IFN-γ) were determined. In addition, for the antioxidant status we measured total antioxidant capacity (TAC) and interleukin-10 (IL-10). Our results demonstrated that the rats had mild renal impairment consistent with a pre-AKI stage due to the nephrotoxic effect of gentamicin. However, TOS, MDA and NO were significantly higher in the gentamicin group compared to the control group. In addition, TAC was higher in the control group. Hence, OS markers reach higher levels and may potentially be used as markers of kidney damage even in cases of mild renal function impairment.

Perspectives of gold nanoparticles and their applications in pancreatic cancer (Review).

Nanoparticles (NPs) represent a major point of interest in the scientific field, with an increasing number of studies revealing promising results. Nano-oncology is a relatively new area of research that continues to expand, revealing new perspectives in both diagnosing and treating cancer. Treating pancreatic cancer (PC) remains a major challenge, with modest positive results, thus an increasing number of studies have focused on this disease. Out of all the NPs that have been used in experimental studies, gold NPs (GNPs) appear to be the most efficient, with little systemic toxicity. This review aims to summarize the latest studies that reveal the effects that GNPs have on PC cells, focusing on different ways in which they can be used to diagnose this disease, to induce apoptosis or cause cytotoxicity in cancer cells. Although literature has limited data concerning this specific topic, the results are promising. However more studies are required until GNPs can be used in clinical practice.

Mitochondrial nanotargeting in malignancies (Review).

Malignancies represent a burden for the health system worldwide. Treating them represents a challenge through the prism of the cancer cell behaviour and the serious systemic side effects that usually occur. Both traditional (chemotherapy, radiotherapy and surgery) and associated therapies (immunotherapy and hormone therapy) have reached a plateau. The new trend for the management of malignancies includes nanoparticles (NPs) which are studied for both their diagnostic and therapeutical use. NPs can be designed in various ways, many of them targeting mitochondria causing cellular apoptosis. This review summarizes the main characteristics of NPs that are studied in different cancers to highlight their mechanism of action. Since mitochondria play a key role in the cellular homeostasis, they represent the main target for the experimental current studies. While there are NPs approved by the FDA for clinical use, most of them are still under extended research and still need to prove their efficacy and biocompatibility, preferable with minimal systemic side effects.

Oxidative stress as a potential target in acute kidney injury.

BACKGROUND: Acute kidney injury (AKI) is a major problem for health systems being directly related to short and long-term morbidity and mortality. In the last years, the incidence of AKI has been increasing. AKI and chronic kidney disease (CKD) are closely interconnected, with a growing rate of CKD linked to repeated and severe episodes of AKI. AKI and CKD can occur also secondary to imbalanced oxidative stress (OS) reactions, inflammation, and apoptosis. The kidney is particularly sensitive to OS. OS is known as a crucial pathogenetic factor in cellular damage, with a direct role in initiation, development, and progression of AKI. The aim of this review is to focus on the pathogenetic role of OS in AKI in order to gain a better understanding. We exposed the potential relationships between OS and the perturbation of renal function and we also presented the redox-dependent factors that can contribute to early kidney injury. In the last decades, promising advances have been made in understanding the pathophysiology of AKI and its consequences, but more studies are needed in order to develop new therapies that can address OS and oxidative damage in early stages of AKI. METHODS: We searched PubMed for relevant articles published up to May 2019. In this review we incorporated data from different types of studies, including observational and experimental, both in vivo and in vitro, studies that provided information about OS in the pathophysiology of AKI. RESULTS: The results show that OS plays a major key role in the initiation and development of AKI, providing the chance to find new targets that can be therapeutically addressed. DISCUSSION: Acute kidney injury represents a major health issue that is still not fully understood. Research in this area still provides new useful data that can help obtain a better management of the patient. OS represents a major focus point in many studies, and a better understanding of its implications in AKI might offer the chance to fight new therapeutic strategies.