RESUMO
Androgenetic alopecia is the most common form of hair loss in men. The present study was designed to evaluate the hair growth-promoting activity of a preparation of the Adiantum capillus-veneris Linn. [A. capillus-veneris] on albino mice using a testosterone-induced alopecia model. Five groups of albino mice were studied: [A] Testosterone solution only [n=6]; [B] Testosterone + Finasteride solution [2%] [n=6]; [C] Testosterone + vehicle [n=6]; [D] Testosterone + A. capillus-veneris solution [1%] [n=6]; [E] intact control [n=2, without testosterone]. Alopecia was induced in all intervention groups by testosterone 1.0 mg subcutaneous. A. capillus-veneris solution was applied topically to the back skin of animals in the respective group. Hair growth was evaluated by visual observation and histological study of several skin sections via various parameters as follicle density [number of follicles/mm] and anagen/telogen ratio. After 21 days, a patch of diffuse hair loss was seen in animals received testosterone while animals treated with A. capillus-veneris showed less hair loss as compared to those treated with testosterone only. The follicular density observed in the A. capillus-veneris-treated group was 1.92 +/- 0.47, compared to 1.05 +/- 0.21 in testosterone-group and 2.05 +/- 0.49 in finasteride-treated animals. Anagen/telogen ratio was significantly affected by A. capillus-veneris, which was 0.92 +/- 0.06 as compared with 0.23 +/- 0.03 and 1.12 +/- 0.06 for testosterone and finasteride treated groups, respectively. According to visual observation and quantitative data [follicular density and anagen/telogen ratio], A. capillus-veneris was found to possess good activity against testosterone-induced alopecia
RESUMO
Chloroacetaldehyde [CAA] is a chlorination by-product in finished drinking water and a toxic metabolite of a wide variety of industrial chemicals [e.g. vinyl chloride] and chemotherapeutic agents [e.g. cyclophosphamide and ifosfamide]. In this research, the cytotoxic mechanisms of CAA in freshly isolated rat hepatocytes were investigated.CAA cytotoxicity was associated with reactive oxygen species [ROS] formation and glutathione depletion suggesting that oxidative stress contributed to the CAA cytotoxic mechanism. CAA-induced oxidative stress cytotoxicity markers were significantly prevented by antioxidants, ROS scavengers, mitochondrial permeability transition [MPT] pore sealing agents, endocytosis inhibitors, ATP generators and xanthine oxidase inhibitor. In our study the hepatocyte mitochondrial membrane potential was rapidly decreased by CAA which was prevented by antioxidants and ROS scavenger indicating that mitochondrial membrane damage was a consequence of ROS formation. CAA cytotoxicity was also associated with lysosomal membrane rupture. Our findings showed that at least four different intracellular sources including: metabolic enzymes cytochrome P[450] and xanthine oxidase, mitochondrial respiratory chain disruption and lysosomal Haber-weiss reaction, were involved in CAA induced ROS formation and other subsequent cytotoxic events. Our other interesting finding was that the lysosomotropic agents prevented CAA induced mitochondrial membrane potential collapse and mitochondrial MPT pore sealing agents inhibited lysosomal membrane damage caused by CAA. It can therefore be suggested that there is probably a toxic interaction [cross-talk] between mitochondrial and lysosomal oxidative stress generating systems, which potentiates each organelle damage and ROS formation in CAA- induced hepatotoxicity