Objective: To examine sex reversal both by oral and by immersion using 17α-methyltestosterone on the methyltestosterone residual concentration and the organ histopathology of tilapia fish. Methods: This study used oral and immersion treatment methods for sex reversal of tilapia fish and used normal fish as the control and each treatment was repeated 4 times. 17α-methyltestosterone at dosages of 60 mg/kg feed and 0.5 mg/L were used for oral and immersion methods, respectively. In the first step, tilapia fry were reared at 100 L aquaria, with a density of 1 fish/L for 2 months. In the next step, male tilapias were reared at happa (net cage) of (2×1×1) m³ size in the controlled pond, with a density of 30 fish/happa for 3 months. The methyltestosterone residual concentrations were analyzed by one-way analysis of variance and Duncan’s multiple range tests, while organ histopathology was analyzed by descriptive method. Results: Residual concentrations in the serum of methyltestosterone- treated fish were significantly lower than that in normal fish, especially in 4- and 5-month-old tilapias with averages of less than 5 μg/L, while in normal fish was more than 5 μg/L. In the flesh, methyltestosterone residual concentrations showed relatively no significant differences between the oral and immersion treatment groups and methyltestosterone-treated fish remained lower compared to normal fish, except in 5-month-old tilapia. Methyltestosterone-treated tilapia exhibited histopathological changes on gill, liver, kidneys, and intestine organs. Conclusions: Sex reversal either by oral or by immersion has methyltestosterone residual concentration, but does not exceed the limits (5 μg/L or 5 μg/kg) of synthetic steroid on the fish body, although methyltestosterone causes histopathological changes on gill, liver, kidneys, and intestine.

Objectives: This study proves the protective effect of Apis dorsata honey against chronic monosodium glutamate (MSG)-induced testicular toxicity on the Leydig cell necrosis count and malondialdehyde (MDA) serum level in Mus musculus mice. Materials and Methods: In this study, 25 male mice were used and grouped into two large groups: The control group consisting of negative control (C-) and positive control (C+). C+ group was fed with 4 mg/g body weight (gBW) of MSG followed by distilled water. The treatment group consisted treatment 1, treatment 2, and treatment 3 groups with A. dorsata honey dosage 53.82 mg/20 g, 107.64 mg/20 g, 161.46 mg/20 g per os (p.o.), respectively, followed by MSG 4 mg/g BW of MSG p.o. For the difference analysis between the group used the one-way ANOVA test and Duncan test. Results: The result of this study showed that there was a significant difference between the treatment group and control group (p<0.05) in the Leydig cell necrosis count and MDA levels. The highest Leydig cell necrosis count and MDA level were found in C+ with values 13.20 +/- 2.05 cell and 37.08 +/- 9.17 mu mol/L compared to C-, while in the treatment group, T3 showed the lowest Leydig cell necrosis value and MDA level 4.64 +/- 0.55 cell and 14.22 +/- 2.01 mu mol/L compared to the C+ group. Conclusion: It can be concluded that A. dorsata honey could reduce the Leydig cell necrosis number and MDA level of mice (Mus musculus) exposed to MSG.

Introduction: The aim of the study was to describe the process of neuron death in the cerebral cortex caused by embryonic carbofuran exposure. Material and Methods: 81 mouse foetuses from 27 breeding mice were used in the study. Carbofuran was administered by gavage from the 6^th to the 15^th day of gestation to two groups: one at 0.0208 and the other at 0.0417 mg/kg b.w. On the 17^th day, the mice were sacrificed and the foetuses were taken to measure the ROS (malondialdehyde/MDA and superoxide dismutase/SOD) activity in brain tissue, the number of apoptotic embryonic cerebral cortex neurons using a TUNEL assay, and necrotic cells using HE staining. Examination of p53 and caspase 3 expression was done by immunohistochemistry. Data were analysed using analysis of variance (ANOVA) and Duncan’s test. Results: Increased activity of cerebral ROS characterised by significant elevation of the MDA level (P < 0.05), decreased SOD (P < 0.01), increased p53 and caspase 3 expression, and cerebral cortical neuron death either by necrosis or apoptosis (P < 0.05) were found. At the low dose carbofuran increased expression of p53, caspase 3, and apoptosis. At the high dose it increased levels of MDA and necrosis. Conclusion: Increased expression of p53 and caspase 3 and apoptosis indicated that carbofuran may cause apoptosis through the intrinsic pathway. The increased apoptosis grants an opportunity to prevent and treat the effect of ROS due to gestational carbofuran exposure.

This study aimed to assess the level of testicular damage by observing the changes in the diameter and epithelium thickness of seminiferous tubules in rats that exposure to nicotine per inhalation. Thirty adult male rats were used and divided into five equal groups and treatment as follows for 20 days; Control group NaCl 0.9%, P1 nicotine 0.5 mg/kg, P2 nicotine 1.0 mg/kg, P3 nicotine 2.0 mg/kg and P4 nicotine 4.0 mg/kg. All groups were given treatment per inhalation for twenty days. At the end of treatment and the rats were sacrificed testes were collected for histopathological preparation. The testes were processed for routine paraffin embedding and staining and the sections were examined for histopathological changes. There results showed that nicotine administration induced varying degrees of structural damage to the seminiferous tubules, as the decreased in diamater and epithelium thickness of seminiferous tubules. The diameter and epithelium thickness of seminiferous tubules in four experimental groups reduced compared to the control group. This study proves that nicotine administration does decreases the spermatogenesis of rats by reducing the diameter and epithelium thickness of seminiferous tubules in testes. It also proves that the level of testicular damage is directly proportional to the dosage of nicotine administrated to male rats.