Comparison of the effect of amino acids and their derivatives on the growth of some dermatophytes: an in vitro study

Background and Aims: Amino acids have different effects on the growth of some dermatophytes. Some may increase whereas others maydecrease their growth. The concentration of some amino acids is also an important factor for their effects

Materials and Methods: To investigate the effects of L-amino acids on the growth of six species of dermatophytes including Epidermophyton floccosum, Microsporum gypseum, Microsporum canison, Trichophyton rubrum, Trichophyton schoienlinii and Trichophyton verrucosum, two concentrations [1 and 0.1 mg/ml] of the 23 L-amino acids and some of their derivatives were added to sabouraud glucose agar media of these dermatophytes. The experiment was carried out three times. After 3 weeks for Trichophyton verrucosum and Trichophyton schoenleinii, and 2 weeks for the rest of dermatophytes, the mean diameter of each colony was measured and compared with the control whose media was not treated with amino acids

Results: The results showed the higher inhibitory effects of L-Cysteine hydrochloride, L-Cysteine, L-Aspartic acid, L-Glutamic acid, DL-Tryptophan and L-Tyrosine on the studied dermatophytes. The other amino acids had less inhibitory or even stimulatory effects on the growth of the dermatophytes

Conclusions: By using the properties of these effective amino acids, antifungal drugs may be synthesized more effective with lower cost and less side effects against different dermatophytes

Zinc and low-dose of cadmium protect sertoli cells against toxic-dose of cadmium: the role of metallothionein

The impact of cadmium [Cd] on male infertility may be related to the interaction with metal-binding proteins known as metallothioneins [Mts]. Trace elements like zinc [Zn] have protective effects on testicular damage induced by Cd. We determined the effect of Zn and low-dose Cd pre-treatment on the expression of Mt1 and Mt2 genes on testicular Sertoli cells. The cultured TM4 mouse sertoli cells were treated with 50 micro M ZnSO4 [Zn pre-treated group; ZnPG], 2 micro M CdCl2 [Cd pre-treated group; CdPG], or distilled water [DW pre-treated group; DWPG]. After 18 hour, all of these groups were exposed to 100 micro M CdCl2 for different periods of time [1, 2, 3, and 6 hours]. There was also a control group for all three groups, which was treated only with distilled water [without Cd or Zn pre-treatment]. Cellular viability, Zn and Cd concentrations and gene expression were assessed by MTT, atomic absorption spectrometry and real time PCR methods, respectively. The expression of Mt1 and Mt2 genes in ZnPG, CdPG, and DWPG was greater than the control group [p=0.02 and p=0.01, respectively]. Cd concentrations in CdPG and DWPG were greater than the control group [p=0.00]. Expression of both genes in ZnPG and CdPG increased after 3 hours of treatment and Cd concentration decreased simultaneously, which was more obvious in ZnPG. Zn and short term low-dose Cd pre-treatment might reduce the adverse effects of Cd by increasing expression of Mts genes in Sertoli cells. The protective effect of Zn was stronger than Cd

Angiotensin II differentially induces matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 production and disturbs MMP/TIMP balance

Angiotensin II, the main component of the rennin-angiotensin system, is associated with cardiovascular diseases such as hypertension, vascular remodeling and inflammation. Remodeling process results from dysregulation of Matrix Metalloproteinases [MMPs] and their tissue inhibitors [TIMPs]. MMPs are considered as important target genes for angiotensin II. The aim of this study was to determine the effects of angiotensin II on MMP-9 and TIMP-1 production and MMP/TIMP balance in a monocytic cell type. Human monocytic U-937 cells were cultured and treated with 100 nM angiotensin II. Supernatants were analyzed for MMP-9 and TIMP-1 using ELISA and zymography methods. Real-time PCR was utilized to evaluate relative MMP-9 and TIMP-1 genes expression following treatments. Cytotoxicity potentials of treatments were determined by assaying lactate dehydrogenase leakage from the cells. Stimulation of the monocytic cells with angiotensin II significantly increased MMP-9 and TIMP-1 secretion as measured by ELISA [p<0.05]. It also augmented gelatinolytic activity of MMP-9 in the conditioned media as much as 49% [p<0.05]. Incubation of the cells with angiotensin II for 12 hr increased MMP-9 and TIMP-1 gene expression 2.7 and 1.8 folds, respectively [p<0.05]. Angiotensin II treatments did not establish significant cytotoxic effects. In summary, our data provide further evidences that monocytic MMP-9 is a major effector of angiotensin II. It is induced more efficiently than TIMP-1 by angiotensin II that leads to MMP/TIMP imbalance. Our data also reveal by the pivotal participation of these cells in pathological cardiovascular remodeling mediated by angiotensin II

Endothelial nitric oxide synthase gene Glu298Asp polymorphism in patients with coronary artery disease

Endo-derived nitric oxide [NO] is synthesized from L-arginine by endothelial nitric oxide synthase [NOS3]. Since reduced NO synthesis in endothelial cells has been implicated in the development of coronary atherosclerosis, we investigated the association of NOS3 gene polymorphisms and coronary artery disease [CAD] in an Iranian population. We studied the NOS3 gene Glu298Asp polymorphism in 241 CAD patients with positive coronary angiograms [i.e., >50% stenosis affecting at least one coronary vessel] in Shahid Rajaee Heart Hospital and 261 control subjects without a history of symptomatic CAD. The NOS3 gene polymorphism was analyzed by polymerase chain reaction and restriction fragment length polymorphism. Lipid profile and other risk factors were also determined. The genotype frequencies of Glu298Asp polymorphism for Glu/Glu, Glu/Asp, and Asp/Asp were 61.3%, 32.2%, and 6.5%, respectively, in control subjects, and 46.5%, 42.7%, and 10.8% in CAD patients, respectively. The genotype frequencies differed significantly between the two groups [P=.003]. The frequencies of the Asp alleles were 32.2% and 22.6% for CAD patients and control subjects, respectively; the difference between the two groups was statistically significant [P=.001; odds ratio=1.6]. Plasma lipids, except HDL-C, were also significantly increased in the CAD groups. These results suggest that CAD is associated with Glu298Asp polymorphism of the NOS3 gene in our population and that this polymorphism is an independent risk factor for CAD