Capsaicin modulates pulmonary antioxidant defense system during benzo(a)pyrene-induced lung cancer in Swiss albino mice

The effect of a pungent ingredient of red pepper, capsaicin, on oxidative stress induced changes in the antioxidant defense system by benzo(a)pyrene in the lungs of mice was studied. Oral gavage administration of benzo(a)pyrene (50 mg/kg body weight) to mice led to a marked increase in oxidative stress indicated by alterations in pulmonary lipid peroxidation, enzymic antioxidants (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase and glucose-6-phosphate dehydrogenase) and non-enzymic antioxidants (reduced glutathione, vitamin C, vitamin E and vitamin A). Pre-co-treatment with capsaicin (10 mg/kg body weight i.p.) restored cellular normalcy, highlighting the antioxidant potential of capsaicin in mitigating the oxidative stress mediated damage produced during benzo(a)pyrene-induced lung cancer.     

Higher Levels of Cystatin C in HIV/AIDS Patients with Metabolic Syndrome

Data about Cystatin‐C levels in HIV‐infected patients with metabolic syndrome (MetS) are still limited. Therefore, the aim of this study was to evaluate the possible correlations of serum levels of Cystatin‐C in HIV/AIDS patients treated with combined antiretroviral therapy (cART) with or without MetS. This cross‐sectional study included 89 HIV/AIDS Caucasian patients receiving cART at the HIV/AIDS Centre Belgrade, Serbia, divided into two groups according to the presence of MetS. Cystatin‐C and other biochemical parameters were measured using Cytokine‐Array‐I, Metabolic‐Array‐I and Metabolic‐Array‐II, at the Department of Clinical Biochemistry, Royal Free Hospital and University College London, UK. A linear regression model was performed to evaluate which clinical and laboratory variables had an independent effect on Cystatin‐C levels in HIV/AIDS patients. There were 33 (37%) patients with MetS and 56 (63%) without MetS. Patients with and without MetS were homogenous for age, duration of cART, number of cART combinations and CD4⁺ T cell count. Statistically increased Cystatin‐C levels were observed in HIV/AIDS patients with MetS (p = 0.017), when compared to patients without MetS. Data showed a positive correlation of Cystatin‐C and C‐reactive protein (r = 0.349, p = 0.001). Using linear regression modelling, significant correlations were obtained between Cystatin‐C and MetS in univariate analysis (p < 0.001). Cystatin‐C levels were significantly higher in HIV/AIDS patients with MetS versus without MetS. Early assessment of MetS using Cystatin‐C as a marker may ultimately help increase the lifespan of HIV/AIDS patients, as these patients appear to be at high risk of cardiovascular diseases.     

Comparison of serum FSH and Inhibin B levels between adult male dizygotic and monozygotic twins

BACKGROUND: FSH hypersecretion occurs in mothers of dizygotic (DZ) twins. Twinning is inherited via both sexes and transmitted through the female. FSH hypersecretion may thus occur in male DZ twins. METHODS: We assayed FSH and its counter-regulatory hormone, Inhibin B, in 108 adult male DZ and 100 monozygotic (MZ) twins (as controls) and compared our results to published norms. RESULTS: Inhibin B was elevated and higher in DZ compared with MZ twins with similar FSH. CONCLUSION: The normal FSH: Inhibin B endocrine feedback axis is different in adult male DZ twins. This contributes to the theory that the answer to human DZ twinning lies in the actions of FSH and Inhibin, and in their mutual interaction.     

Beneficial influence of capsaicin on lipid peroxidation, membrane-bound enzymes and glycoprotein profile during experimental lung carcinogenesis

This study was designed to examine the impact of a principal component of hot red peppers and chilli peppers, capsaicin, on alterations in lipid peroxidation, membrane-bound enzyme profiles and glycoprotein levels during benzo(a)pyrene (BP)-induced lung cancer in Swiss albino mice. BP (50 mgkg(-1)) induced deleterious changes that were that revealed by alterations in lipid peroxidation, membrane-bound enzyme (Na+/K+ ATPase, Ca2+ ATPase and Mg2+ ATPase) activity, levels of total protein and protein-bound carbohydrate components (sialic acid, hexose, hexosamine, hexuronic acid and fucose). Pre-co-treatment with capsaicin (10 mg kg(-1)) restored the detrimental effects induced by BP, indicating its protective role in BP-induced lung cancer.     

Carvacrol Promotes Cell Cycle Arrest and Apoptosis through PI3K/AKT Signaling Pathway in MCF-7 Breast Cancer Cells

Objective: To examine the role of carvacrol in modulating PI3K/AKT signaling involved in human breast cancer pathogenesis using in vitro experimental model MCF-7 cells. Methods: MTT and lactate dehydrogenase assays were performed with cells treated with different doses of carvacrol (0–250 μ mol/L) at different time points (24 and 48 h). The nuclear morphology was assessed in MCF-7 cells with propidium iodide (PI) and acridine orange/ethidium bromide (AO/EB) staining and analyzed by fluorescence microscopy. Events like cell cycle arrest and apoptosis were observed by flow cytometric analysis and expressions of p-Rb, cyclin D1, cyclin-dependent kinase 4 (CDK4), CDK6, Bax, Bcl-2, PI3K/p-AKT were analyzed by immunoblot. Results: Carvacrol significantly reduced cell viability with the half maximal inhibitory concentration value of 200 μ mol/L at 24 and 48 h (P<0.05). importantly, there was a significant increase in the accumulation of the G0/G1 phase upon treatment with carvacrol in MCF-7 cells (P<0.05 or P<0.01). A remarkable decrease in protein expressions of p-Rb, cyclin D1, CDK4 and CDK6 denoted cell cycle arrest (P<0.05 or P<0.01). In addition, carvacrol treatment significantly inhibited PI3K/p-AKT protein expressions leading to induction of apoptosis mediated by decreased Bcl2 and increased Bax protein expressions. Further, Annexin V/PI staining by FACS analysis, dual staining by AO/EB and PI staining studies suggested induction of apoptosis by carvacrol through PI3K/Akt signaling pathway in MCF-7 cells. Conclusion: Carvacrol significantly inhibited the breast cancer MCF-7 cell proliferation and induced apoptosis via suppressing PI3/AKT signaling pathway.