Slopain said:
My lord, you are on CRACK
I am not on crack. I have the personal opinion that testosterone isn't a good steroid. THis is from my own experience with it. Some people like it, I don't. I also don;t like antiestrogens, the way they make you feel and what i have read about how they react with the body. On top of it all they don't even work 100 percent of the time to eliminate gyno if enough testosterone is used. I like non aromatizing steroids. I don't like estrogen or fake estrogen either.
HEre is why nolva is bad for you:
Italian National Cancer Institute, G. Pascale Foundation, Naples.
[email protected]
The antiestrogen tamoxifen (TAM) is widely used as a drug against breast cancer and is currently being tested as a chemopreventive agent. However, a number of studies showed genotoxic and carcinogenic effects of TAM. These effects are thought to be related to oxygen radical overproduction which occurs during TAM metabolic activation. There is no evidence, thus far, on TAM toxicity to embryos and gametes. The present study was designed to elucidate the mechanisms of TAM-induced developmental, reproductive and cytogenetic toxicity towards sea urchin (SU) embryos with regard to the possibility of TAM-initiated oxidative stress. Embryo cultures from SU were subjected to long-term (throughout embryogenesis) or short-term (two hours) incubation with TAM at concentrations from 10(-8) to 10(-5) M. The experiments on TAM-induced toxicity to gametes were carried out with SU sperm, or unfertilized eggs, suspended in TAM (10(-8) to 10(-6) M). To assess the effects of TAM to embryos or to gametes, developmental defects, embryonic mortality, fertilization success, and cytogenetic abnormalities were scored. Oxidative damage to DNA and lipids was detected by measurements of 8OHdG levels and lipid peroxidation, respectively. Reactive oxygen species (ROS) production by eggs and embryos was recorded by luminol-dependent chemiluminescence (LDCL) and cytochrome c reduction methods. The changes in activities of SU superoxide dismutase (SOD) and catalase were also evaluated. TAM exerted: a) early embryonic mortality to exposed embryos and to the offspring of exposed eggs; b) developmental defects to the offspring of exposed sperm; c) decrease in sperm fertilization success, and d) cytogenetic effects in the offspring of exposed sperm or eggs. These morphological effects corresponded to the state of oxidative stress in SU embryos (increased oxidative damage to DNA and lipids and induction of antioxidant enzymes). Since TAM did increase significantly ROS production by embryos, it is suggested that TAM may be metabolically activated by SU embryonic oxidases and peroxidases, which in turn could be induced by TAM. The present study provides further support to the utilization of the SU system as a useful model to help elucidate mechanisms of chemical teratogenesis and carcinogenesis.
Division of Toxicology, Whitaker College of Health Sciences and Technology, Massachusetts Institute of Technology, Cambridge 02139-4307, USA.
Tamoxifen was carcinogenic to the liver of male and female rats, inducing hepatocellular carcinomas when administered daily by gavage or fed continuously in the diet. It also acted as a promoting agent in a two-stage model of carcinogenesis in rat liver. In contrast, tamoxifen acted as a protective agent in abrogating estrogen-induced hepatotoxicity and hepatocarcinogenesis in hamsters. Tamoxifen did not induce malignancies in mice when administered according to dosing protocols that are effective in inducing hepatocellular carcinomas in rat liver. In the rat, tamoxifen is metabolized to alpha-hydroxytamoxifen, which is further activated to a product that binds principally to the exocyclic amino group of deoxyguanosine in DNA. The same adduct pattern is formed in mouse hepatocytes treated with tamoxifen or its alpha-hydroxylated derivative, and in human hepatocytes exposed to the latter metabolite. However, available data indicate that human cells have a substantially lower capacity than rodent cells for activation of tamoxifen. Tamoxifen also induces aneuploidy in rat hepatocytes in vivo. This evidence has led some investigators to characterize tamoxifen as a carcinogen that acts through both genotoxic and nongenotoxic mechanisms, with the implication that women treated with the drug may be consequently subjected to elevated risk of cancer, particularly of the endometrium. Critical examination of the evidence, however, indicates that extrapolation of these experimental data to humans is subject to very substantial uncertainty. Available data clearly indicate major differences between women and rats with respect to the activation of tamoxifen and formation of DNA adducts, and bring into question the validity of direct extrapolation of data generated in the single susceptible species, the rat, to women in assessing potential risks attendant to tamoxifen administration.
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