I'm such an AAS geek. between watching the masters today I've been reading more studies on tren. i should get a life huh?
here are some interesting things in studies from those german scientists on that link i posted on tren's effects.
Twenty heifers which were each administered 3 or 4 implants containing trenbolone acetate were slaughtered at 30 days post-implantation. Liquid chromatographic analyses were conducted on muscle collected from the rump, loin, shoulder, and neck, and on the liver of each animal. Residues present in liver were primarily 17alpha-trenbolone, and the residues found in the various muscle samples were primarily 17beta-trenbolone. The mean concentration of 17alpha-trenbolone in liver was 4.3 +/- 2.3 ng/g; the mean concentration of 17beta-trenbolone in muscle tissues was < 0.4 ng/g. There was a small but statistically significant effect of the number of implants used on the mean concentration of residues in loin muscles; animals with 3 trenbolone implants had higher mean residue concentrations than animals with 4 trenbolone implants. This suggests that, though the impact of implant numbers on the mean concentration of residues in muscle tissues is negligible relative to currently generally accepted maximum residue levels, mechanisms may exist for selective distribution and retention of residues within different muscle groups.
Recently, a growth promoter for farm animals, trenbolone acetate, was identified as an environmental androgen that potentially affects reproduction. Because androgens also suppress immunity, it was hypothesized that an active metabolite of trenbolone acetate, 17beta-trenbolone (TB), might impair immune responses. Castrated adult CD-1 mice were injected daily with either one of two different doses of 17beta-trenbolone (TB), testosterone propionate (TP), or corn oil (vehicle). The antigen-specific immune response was assessed by measuring delayed-type hypersensitivity (DTH) responses. Reproductive response was assessed by measuring reproductive tissue mass and determining testosterone concentrations. Mice treated with TB or TP displayed larger reproductive tissue mass than males treated with corn oil. Furthermore, males exposed to the highest dose of TB displayed a reduced DTH response compared to vehicle-treated animals. In comparison, TP, at a similar dose, only minimally reduced the DTH response. These data support the reproductive and potentially immunosuppressive effects of this environmental androgen, and raise the possibility of health concerns for individuals or populations in contact with high concentrations of TB
Angus and Angus x Limousin cross steers (n = 182; initial BW = 309 +/- 27.8 kg) were used to evaluate the influence of an estradiol-trenbolone acetate implant (containing 24 mg of estradiol and 125 mg of trenbolone acetate) on production efficiency and carcass traits when administered at specific stages of growth. Treatments were 1) control, no implant (NI); 2) early implant (EI) on d 1 (BW = 309 kg); or 3) delayed implant (DI) on d 57 (BW = 385 kg). Comparisons were also made between the NI and implanted treatments (I; EI + DI). Steers were procured at weaning and were backgrounded (47 d) before the initiation of the experiment. Initial predicted carcass composition was 14.9% protein, 13.3% fat, 54.6% moisture, and 17.2% bone. Days on feed were constant across treatment. After 56 d, ADG and G:F were improved (P < 0.01) by implants, NI vs. EI (1.68 vs. 1.90 kg and 0.227 vs. 0.257). At d 57, predicted carcass composition did not differ among treatments. From 57 to 112 d, DI caused higher ADG than NI or EI (NI = 1.65, EI = 1.57, and DI = 1.78 kg; P < 0.05) and higher G:F (NI = 0.155, EI = 0.150, and DI = 0.173; P < 0.01). Cumulative ADG and G:F were improved by implants (1.65 vs. 1.73 kg; P < 0.05) and (0.175 vs. 0.186; P < 0.01) for NI vs. I, respectively, with no differences between treatments that involved implants. Cumulative DMI was similar for all treatments. Implanting increased dressing percentage (63.5 vs. 64.1%; P < 0.05) and increased (P < 0.01) hot carcass weight (341 vs. 353 kg) and LM area (76.5 vs. 81.4 cm(2)) for NI vs. I, respectively. Rib fat and kidney, pelvic, and heart fat were not affected by treatment, and treatment had no effect on the whole carcass proportions of fat, protein, or water. Implants advanced maturity scores (NI = A(51) vs. EI + DI = A(59); P < 0.01). Marbling scores were decreased (P < 0.05) by EI but not by DI (NI = Small(65), EI = Small(20), DI = Small(36)). The percentage of i.m. fat content of the LM was decreased (P < 0.10) by EI and was not affected by DI (NI = 5.1, EI = 4.0, DI = 4.8%). Treatment affected (P < 0.10) the proportion of carcasses with marbling scores greater than Modest(0) (NI = 23.6, EI = 7.8, DI = 22.6%). The results of this study suggest that growth of i.m. fat is sensitive to anabolic growth promotants administered during early periods of growth.
Environmentally relevant concentrations of 17beta-trenbolone cause a strong and irreversible masculinization of zebrafish and that raises concern about the effects of androgenic discharges in the aquatic environment. In addition this study also aids in understanding of the so far unknown sex determination process in zebrafish.
17beta-Trenbolone is a metabolite of trenbolone acetate, an anabolic steroid used as a growth promoter in beef cattle. 17beta-Trenbolone in runoff from cattle feedlots may reach concentrations that affect fish sexual development. Zebrafish were exposed to a concentration of 20 ng/L TB in a flow-through system for five months from egg until sexual maturity. This resulted in an all-male population. It was further found that all these phenotypic males displayed normal male courtship behavior and were able to reproduce successfully, implying that the sex reversal was complete and functional. None of the phenotypic males developed into females after six months in clean water, demonstrating that androgenic sex reversal of zebrafish is irreversible.
Please Scroll Down to See Forums Below 
