Background The present research aimed to analyze the impacts of magnesium and zinc supplements on glycemic control, serum lipids, and biomarkers of oxidative stress and inflammation in patients suffering from coronary heart disease (CHD) and type 2 diabetes mellitus (T2DM). Methods According to the research design, a randomized, double-blind, placebo-controlled trial has been implemented on 60 subjects suffering from CHD and T2DM. Therefore, participants have been randomly divided into 2 groups for taking placebo (n = 30) or 250 mg magnesium oxide plus 150 mg zinc sulfate (n = 30) for 12 weeks. Results Magnesium and zinc significantly decreased fasting plasma glucose (FPG) (β − 9.44 mg/dL, 95% CI, − 18.30, − 0.57; P = 0.03) and insulin levels (β − 1.37 μIU/mL, 95% CI, − 2.57, − 0.18; P = 0.02). Moreover, HDL-cholesterol levels significantly enhanced (β 2.09 mg/dL, 95% CI, 0.05, 4.13; P = 0.04) in comparison to the placebo. There was an association between magnesium and zinc intake, and a significant decrease of C-reactive protein (CRP) (β − 0.85 mg/L, 95% CI, − 1.26, − 0.45; P < 0.001), a significant increase in total nitrite (β 5.13 μmol/L, 95% CI, 1.85, 8.41; P = 0.003) and total antioxidant capacity (TAC) (β 43.44 mmol/L, 95% CI, 3.39, 83.50; P = 0.03) when compared with placebo. Furthermore, magnesium and zinc significantly reduced the Beck Depression Inventory index (BDI) (β − 1.66; 95% CI, − 3.32, − 0.009; P = 0.04) and Beck Anxiety Inventory (BAI) (β − 1.30; 95% CI, − 2.43, − 0.16; P = 0.02) when compared with the placebo. Conclusions In patients with T2DM and CHD, the 12-week intake of magnesium plus zinc had beneficial effects on FPG, HDL-cholesterol, CRP, insulin, total nitrite, TAC levels, and BDI and BAI score. This suggests that magnesium and zinc co-supplementation may be beneficial for patients with T2DM and CHD. Further studies on more patients and lasting longer are needed to determine the safety of magnesium and zinc co-supplementation. Trial registration Current Controlled Trials http://www.irct.ir: IRCT20130211012438N31 at 11 May 2019 of registration. This study retrospectively registered.

Today, it has been proven that the nanoparticles such as superparamagnetic iron oxide nanoparticles (SPIONs) have widespread use in biomedical applications, for instance, in magnetic resonance imaging and targeted delivery of drugs. Despite many studies on SPIONs in diagnosing some diseases like cancer, it has not been investigated on the oral tongue squamous cell carcinoma (OTSCC) detection by the NPs. Hence, the present study has been designed to assess the in vitro cytotoxicity of SPIONs on the isolated mitochondria of OTSCC by mitochondrial tests. Isolated mitochondria were removed from the separated cancer and control tissues from the squamous cells of tango in male Wistar rats (6 or 8 weeks) and exposed to the different concentrations of SPIONs (30, 60, and 120 nM). A rise in the production of reactive oxygen species is one of the significant mechanisms of this study, followed by a collapse of mitochondrial membrane potential, the escape of mitochondrial cytochrome c, and mitochondrial swelling in the exposed isolated mitochondria of OTSCC with SPIONs. Furthermore, our results indicated that the exposure to the SPIONs reduced the activity of succinate dehydrogenase in complex II of the mitochondria obtained from cancerous oral tongue squamous. So the SPIONs can induce selective cytotoxicity on the OTSCC mitochondria without significant effects on the control mitochondria. Based on the results and further studies about in vivo experiments in this regard, it is concluded the SPIONs may be a hopeful therapeutic candidate for the treatment of OTSCC. K E Y W O R D S cytotoxicity, mitochondria, oral tongue squamous cell carcinoma, oxidative stress, superparamagnetic iron oxide nanoparticles 1 | INTRODUCTION Oral tongue squamous cell carcinoma (OTSCC) is the most common malignancy of the oral cavity. The incidence of OTSCC is increasing, [1,2] and it has an aggressive clinical behavior with a relatively poor prognosis. [3] The most important risk factors for the development of OTSCC and tongue and oral cavity cancer are tobacco and alcohol; however, tobacco is more carcinogenic than alcohol. [4-7] It has been Jahanfar Jahanbani and Maryam Ghotbi equally share the position of 1st author in this article.

Background: The present research aimed to analyze the impacts of magnesium and zinc supplement on the metabolic level in the patients suffering from CHD (coronary heart disease) and T2DM (type 2 diabetes mellitus). Methods: According to the research design, a randomized, double-blind, placebo-controlled trial has been implemented on 55 women suffering from CHD and T2DM. Therefore, the participants have been randomly divided into 2 groups for taking placebo (n = 28) or 250 mg magnesium oxide plus 220 mg zinc sulfate (n =27) or for 12 weeks. Results: Magnesium and zinc considerably declined the levels of fasting plasma glucose (FPG) (β -9.44 mg/dL, 95% CI, -18.30, -0.57; P = 0.03) and levels of insulin (β -1.37 µIU/mL, 95% CI, -2.57, -0.18; P = 0.02). Moreover, levels of HDL-cholesterol have been remarkably enhanced (β 2.09 mg/dL, 95% CI, 0.05, 4.13; P = 0.04) in comparison to the placebo. There have been an association between magnesium and zinc intake and a considerable decrease of C-reactive protein (CRP) (β -0.85 mg/L, 95% CI, -1.26, -0.45; P < 0.001), a considerable enhancement in the total nitrite (β 5.13 µmol/L, 95% CI, 1.85, 8.41; P = 0.003), and total anti-oxidant capacities (TAC) (β 43.44 mmol/L, 95% CI, 3.39, 83.50; P=0.03) in comparison to the placebo. Furthermore, magnesium and zinc remarkably reduced the Beck Depression Inventory index (BDI) (β -1.66; 95% CI, -3.32, -0.009; P = 0.04) and Beck Anxiety Inventory (BAI) (β -1.30; 95% CI, -2.43, -0.16; P=0.02) in comparison to the placebo. Conclusions: In patients with T2DM and CVD the 12-week intake of magnesium and zinc affected FPG, HDL-cholesterol, CRP, insulin, NO, TAC levels, and BDI and BAI score usefully. Trial registration: Current Controlled Trials http://www.irct.ir: IRCT20130211012438N31 at 11 May 2019 of registration. This study retrospectively registered.