Cytotoxic Effects of Pistacia khinjuk Seed Extracts on Different Cell Lines and its Mitogenic Effects on Blood Lymphocyte In Vitro

Reports indicated that extract Pistacia khinjuk has anti-inflammatory, antipyretic, antibacterial, and antiviral, in treating of diarrhea and throat infections and has hepatoprotective effects against acetaminophen and carbon tetrachloride. This study was undertaken to investigate the possible cytotoxic effects of methanolic and aqueous seeds extract of P. khinjuk on different tumors (rhabdomyosarcoma [RD] and murine mammary adenocarcinoma [Ahmed-Mohammed-Nahi-2003 (AMN-3)]) and normal cell lines (murine fibroblast) and its mitogenic effects on blood lymphocytes. The cytotoxic effects of P. khinjuk seed extracts were evaluated on two tumor cell lines, RD and murine mammary adenocarcinoma (AMN-3) and one normal cell line, murine fibroblast (L20B). Moreover, the mitogenic effects of the plant extract were studied, on human blood lymphocytes. Both methanolic and aqueous seed extracts of P. khinjuk significantly induced tumor cell lines and the normal cell line proliferation, especially in highest concentrations. The results show that the extracts induced significant increases in human blood lymphocyte proliferation at 72 h. This activity of plant extracts recommends it as a good mitogenic agent in researches; in conclusion, seed extracts of P. khinjuk induced proliferation of all tested cell lines. High concentrations of both aqueous and methanolic seed extracts of P. khinjuk showed mitogenic effects

Drug metabolism and cytochrome P-450 (CYPs)

Cytochrome p-450 (CYPs) convert xenobiotics, chemicals, and drugs in the liver into intoxic materials that can be easily eliminated in the body. However, these CYPs sometimes mediate fatal diseases by converting drugs (for instance, paracetamol) into toxic substances that cannot be eliminated or excreted quickly from the body and hence cause hepatocyte damage that decreases the function of the liver. This article review aimed to determine the history, nomenclature, family, and subfamily of CYPs and mainly stress cytochrome P450 roles in drug metabolism. Some toxic byproducts induce autoreactive antibodies by binding to the CYPs, which causes further damage to hepatocytes. The most common causes of liver damage are type II autoimmune hepatitis, drinking alcohol, and free radicals, which cause DNA mutations. Another condition that leads to liver damage is the inability of the liver to detoxify the drug, which leads to further damage to the liver. There are some isoforms of CYPs, such as 3A, 1A, and 2C19, that are severely affected when the liver is no longer able to relieve toxic products, but some isoforms of CYPs are less affected during damage to the liver, which includes 2E1, 2D6, and 2C9. There are parameters for the involvement of CYPs in liver disease, depending on the cause of the damage, which is either drugs or alcohol. Thus, further research must be done to know the exact etiology and management of the diseases related to liver damage through CYPs

Cardiovascular effects of vitexin isolated from Prosopis farcta

Vitexin was isolated and identified from fruit of Prosopis farcta (Iraqi indigenous). Cardiovascular actions of vitexin were studied in vitro and in vivo. Vitexin produced a positive inotropic effect on isolated atrium of the rabbit which was not related to Beta 1 adrenergic receptor activation. Vitexin had no vasodilator activity nor it could reverse the vasoconstrictor responses of the isolated pulmonary artery of the rabbit to potassium chloride and phenylephrine.vitexin has produced a significant increase in urine flow and urinary sodium and potassium excretions in healthy and mild hypertensive volunteers and in rabbit. Moreover, vitexin significantly reduced mean arterial blood pressure of the mild hypertensive volunteers and rabbits. This hypotensive effect of vitexin is not related to a direct vasodilatation or to blocking alpha and Beta adrenergic receptors. The most likely mechanism of action of vitexin as a hypotensive compound is through its diuretic effects

Assessment of Nitrofurantoin as an Experimental Intracanal Medicament in Endodontics

Background and Objectives. Multiple antibacterial agents have been mixed and used as an intracanal medicament-like modified triple antibiotic paste (MTAP) to eliminate Enterococcus faecalis (EF), which has been most frequently identified in the cases of failed root canal treatment and periapical lesions. This study is aimed at using a single antibacterial agent, nitrofurantoin (Nit), as an experimental intracanal medicament paste against different clinical isolates of EF bacteria and at comparing its antimicrobial efficacy with MTAP. Materials and Methods. Three strains of EF (S1, S2, and S3) were clinically isolated. A total of 198 straight single-rooted human teeth were collected and divided randomly into three main groups: group N (Nit) (n=90), group M (MTAP) (n=90), and group W (distilled water) (n=18). The main groups were subdivided into three subgroups according to the strain of EF: in groups N and M, subgroups S1, S2, and S3 (n=30), while in group W, subgroups S1, S2, and S3 (n=6). Then, each subgroup of N and M was divided into five groups (n=6) according to the concentrations of Nit or MTAP (6.25, 12.5, 25, 50, and 100 mg/mL). The colony-forming unit (CFU) of EF from the canal lumen and dentinal chips was measured. Results. Nit could eradicate S1, S2, and S3 completely with concentrations of 6.25, 12.5, and 25 mg/mL, respectively, while MTAP showed complete eradication of the three strains only at 25 mg/mL. In all the groups, it was found that the CFU counts of EF in the dentinal chips were higher than those in the root canal lumen. Conclusion. At the concentration of 25 mg/mL, the Nit paste is effective in eradicating EF completely when it is used as an intracanal medicament