Prevalence of Iatrogenic Vitamin D Toxicity Among the Saudi Population of Vitamin D Users Due to Overcorrection.

Background Despite abundant sunlight exposure, vitamin D deficiency remains a major challenge in Saudi Arabia. Meanwhile, the widespread use of vitamin D supplements has prompted concerns about toxicity, which although rare, can have severe health consequences. Objective The objective of this cross-sectional study was to analyze the prevalence and associated factors of iatrogenic vitamin D toxicity among the Saudi population of vitamin D users due to overcorrection. Methods An online questionnaire was used to collect data from 1,677 participants across all regions of Saudi Arabia. The questionnaire included responses on the prescription, duration of vitamin D intake, dosage, frequency, history of vitamin D toxicity, symptom onset, and duration. Results One thousand six hundred and seventy-seven responses were included across all regions of Saudi Arabia. A majority of participants were female (66.7%) and around half were aged 18-25 years. A history of vitamin D use was reported by 63.8% of participants, and 48% were still using vitamin D supplements. Most participants (79.3%) consulted a physician, and 84.8% had taken a vitamin D test before using the supplement. Commonly reported motives for taking vitamin D included vitamin D deficiency (72.1%), lack of sun exposure (26.1%), and hair loss (20.6%). Symptoms of overdose were reported by 6.6% of participants, with 3.3% having an overdose and 2.1% experiencing both overdose and symptoms. Conclusion This study showed that although a large portion of the Saudi population is taking vitamin D supplements, the prevalence of vitamin D toxicity is relatively low. However, this prevalence should not be ignored, and further research is needed to understand the factors contributing to vitamin D toxicity in order to minimize its occurrence.

Roles of p53 and caspases in induction of apoptosis in MCF- 7 breast cancer cells treated with a methanolic extract of Nigella sativa seeds.

BACKGROUND: Nigella Sativa (NS) is an herb from the Ranunculaceae family that exhibits numerous medicinal properties and has been used as important constituent of many complementary and alternative medicines (CAMs). The ability of NS to kill cancer cells such as PC3, HeLa and hepatoma cells is well established. However, our understanding of the mode of death caused by NS remains nebulous. The objective of this study was to gain further insight into the mode and mechanism of death caused by NS in breast cancer MCF-7 cells. MATERIALS AND METHODS: Human breast cancer cells (MCF-7) were treated with a methanolic extract of NS, and a dose- and time-dependent study was performed. The IC50 was calculated using a Cell Titer Blue® viability assay assay, and evidence for DNA fragmentation was obtained by fluorescence microscopy TUNEL assay. Gene expression was also profiled for a number of apoptosis-related genes (Caspase-3, -8, -9 and p53 genes) through qPCR. RESULTS: The IC50 of MCF-7 cells was 62.8 µL/mL. When MCF-7 cells were exposed to 50 µL/mL and 100 µL/mL NS for 24 h, 48 h and 72 h, microscopic examination (TUNEL assay) revealed a dose- and time-dependent increase in apoptosis. Similarly, the expression of the Caspase-3, -8, -9 and p53 genes increased significantly according to the dose and time. CONCLUSIONS: NS induced apoptosis in MCF-7 cells through both the p53 and caspase pathways. NS could potentially represent an alternative source of medicine for breast cancer therapy.

Apoptosis-mediated inhibition of human breast cancer cell proliferation by lemon citrus extract.

Dietary phytochemicals have a variety of antitumor properties. In the present study, the antitumor activity of methanolic extract of lemon fruit (lemon extract; LE) (LE) on the MCF-7 breast cancer cell line was investigated in vitro. Apoptotic cell death was analyzed using the TUNEL assay. In addition, the apoptosis mediated by LE extract in the MCF-7 cells was associated with the increased expression of the tumor suppressor p53 and caspase-3. Additionally, the expression of a pro-apoptotic gene, bax, was increased, and the expression of an anti-apoptotic gene, bcl-2, was decreased by LE extract treatment, resulting in a shift in the Bax:Bcl-2 ratio to one that favored apoptosis. The expression of a major apoptotic gene, caspase-3, was increased by LE extract treatment. In light of the above results, we concluded that LE extract can induce the apoptosis of MCF-7 breast cancer cells via Bax-related caspase-3 activation. This study provides experimental data that are relevant to the possible future clinical use of LE to treat breast cancer.