Objective Endosulfan is an extremely toxic organochlorine pesticide to aquatic organisms which might be hampering fish health through impairment of metabolism sometimes leading to death.So an experimental protocol was designed to look at endosulfan effects on a number of selected biochemical endpoints as well as to develop a mechanistic understanding of biochemical effects of endosulfan in freshwater fish. Methods The adult freshwater catfish Clarias batrachus were collected and acclimatized to laboratory condition for two weeks prior to experimentation. The toxicity bioassay test of commercial grade endosulfan (35% EC) was conducted for 21 days to determine its initial lethal concentration. The fish were exposed to sublethal concentration of endosulfan (0.06 mg/L) for 21 days. Pesticide - withdrawal experiments were also performed to study recovery. Protein synthesis inhibitors were injected to know the possible mechanism of recovery. The specimens of C. batrachus were sacrificed and brain, liver and caudal white skeletal muscle were removed. Tissues were homogenized and fractions were obtained by differential centrifugation. The activities of citrate synthase (CS), glucose 6-phosphate dehydrogenase (G6-PDH) and lactate dehydrogease (LDH) were assayed spectrophotometrically. Similarly, DNA, RNA and protein content were measured as per standard procedure. Results The exposure of sublethal concentration of endosulfan decreased the activity of citrate synthase (CS) and glucose 6-phosphate dehydrogenase (G6-PDH) in the brain, liver and skeletal muscle of the freshwater catfish, C. batrachus. The brain lactate dehydrogenase (LDH) activity was also reduced in response to endosulfan toxicity. The maximum reduction in activities of these enzyme was 34%-43%. Withdrawal of endosulfan restored the enzyme activity to control level in all the three tissues. The recovery in enzyme activity appears to be due to dissociation of endosulfan or its metabolite(s) from the enzyme molecules and/or fresh synthesis of enzymes. The treatment of actinomycin D or cycloheximide partially inhibited the withdrawal-dependent increase in enzyme activity. This substantiates de novo synthesis of enzyme during recovery period. Since the reduction in enzyme acfvity was more pronounced in response to actinomycin D, endosulfan might be inhibiting the transcription process. But endosulfan did not produce any significant effect on DNA content and RNA/DNA. However, the RNA and protein contents of brain, liver and skeletal muscle decreased significantiy in tissues. The maximum decrease in RNA and protein was approximately 30%-37%. Withdrawal of endosulfan from the medium for 21 days restored the RNA, and protein contents nearly to their control levels. The treatment of actinomycin D or cycloheximide partially inhibited the withdrawal-dependent increase in these macromolecular contents. This effect was more pronounced in case of actinomycin D which again supports the possibility of endosulfan-induced inhibition at transcription level. Conclusion The present study suggests endosulfan-induced impairment of metabolism in fish, which appeared to be due to inhibition of transcription at some unknown points.

Objective: This study was conducted to investigate chromosomal abnormalities and their correlations with clinical and radiological findings in females with primary amenorrhea (PA). Methods: Detailed forms were recorded for 470 females, including the construction of three-generation pedigrees. Peripheral venous blood was drawn, with informed consent, for cytogenetic analysis. Results: An abnormal karyotype was found in 16.38% of participants. The incidence of structural abnormalities (6.8%) exceeded that of numerical abnormalities (6.15%). Turner syndrome represented 45% of all numerical abnormalities. Furthermore, the Y chromosome was detected in 5% of females with PA. Among the structural chromosomal abnormalities detected (n=32) were mosaicism (25%), deletions (12.5%), isochromosomes (18.75%), fragile sites (3.12%), derivatives (3.12%), marker chromosomes (3.12%), and normal variants (29.125%). An examination of secondary sexual characteristics revealed that 29.6% of females had a complete absence of breast development, 29.78% lacked pubic hair, and 36.88% exhibited no axillary hair development. Radiological findings revealed that 51.22% of females had a hypoplastic uterus and 26.66% had a completely absent uterus. Abnormal ovarian development, such as the complete absence of both ovaries, absence of one ovary, one absent and other streak, or both streak ovaries, was observed in 69.47% of females with PA. Additionally 43.1%, 36.1%, 67.4%, and 8% of females had elevated levels of serum follicle-stimulating hormone, luteinizing hormone, thyroid-stimulating hormone, and prolactin, respectively. Conclusion This study underscores the importance of karyotyping as a fundamental diagnostic tool for assessing PA. The cytogenetic correlation with these profiles will aid in genetic counseling and further management of the condition.

This study was conducted to assess the efficacy of subcutaneous granulocyte colony-stimulating factor (G-CSF) for treating thin endometrium. Methods: Data from 88 infertile women with thin endometrium (<7 mm) aged 23 to 40 years were evaluated retrospectively over a period of 1 year. In group 1, subcutaneous infusion of G-CSF (300 μg/mL) was administered to 44 women along with other supplemental treatments. If the lining did not exceed 7 mm within 72 hours, a second infusion was administered. In group 2, which also had 44 women, only estradiol valerate and sildenafil were administered, while subcutaneous G-CSF infusion was not. Embryo transfers were performed once the lining exceeded 7.5 mm. The efficacy of G-CSF was evaluated by assessing the thickness of the endometrium before embryo transfer, pregnancy rates, and clinical pregnancy rates. Results: There were no differences between the groups regarding demographic variables, egg reserves, sperm parameters, the number of embryos transferred, and embryo quality. The pregnancy rate was significantly higher in group 1 (60%, 24 of 40 cases) than in group 2 (31%, 9 of 29 cases) (p<0.001). The clinical pregnancy rate was also significantly higher in group 1 (55%) than in group 2 (24%) (p<0.001). Conclusion: Subcutaneous G-CSF infusion improved the thickness of the endometrium when it was thin. To the best of our knowledge, this is the first documented study to clearly demonstrate the benefits of subcutaneous G-CSF infusion for treating thin endometrium.

Moderate levels of endogenous reactive oxygen species (ROS) are important for various cellular activities, but high levels lead to toxicity and are associated with various diseases. Levels of ROS are maintained as a balance between oxidants and antioxidants. Accumulating data suggest that oxidative stress is a major factor in deterioration of renal function. In this review, we highlight the possible mechanism by which oxidative stress can lead to chronic kidney disease (CKD). This review also describes therapies that counter the effect of oxidative stress in CKD patients. Numerous factors such as upregulation of genes involved in oxidative phosphorylation and ROS generation, chronic inflammation, vitamin D deficiency, and a compromised antioxidant defense mechanism system cause progressive detrimental effects on renal function that eventually lead to loss of kidney function. Patients with renal dysfunction are highly susceptible to oxidative stress, as risk factors such as diabetes, renal hypertension, dietary restrictions, hemodialysis, and old age predispose them to increased levels of ROS. Biomolecular adducts (DNA, proteins, and lipids) formed due to reaction with ROS can be used to determine oxidative stress levels. Based on the strong correlation between oxidative stress and CKD, reversal of oxidative stress is being explored as a major therapeutic option. Xanthine oxidase inhibitors, dietary antioxidants, and other agents that scavenge free radicals are gaining interest as treatment modalities in CKD patients.

Moderate levels of endogenous reactive oxygen species (ROS) are important for various cellular activities, but high levels lead to toxicity and are associated with various diseases. Levels of ROS are maintained as a balance between oxidants and antioxidants. Accumulating data suggest that oxidative stress is a major factor in deterioration of renal function. In this review, we highlight the possible mechanism by which oxidative stress can lead to chronic kidney disease (CKD). This review also describes therapies that counter the effect of oxidative stress in CKD patients. Numerous factors such as upregulation of genes involved in oxidative phosphorylation and ROS generation, chronic inflammation, vitamin D deficiency, and a compromised antioxidant defense mechanism system cause progressive detrimental effects on renal function that eventually lead to loss of kidney function. Patients with renal dysfunction are highly susceptible to oxidative stress, as risk factors such as diabetes, renal hypertension, dietary restrictions, hemodialysis, and old age predispose them to increased levels of ROS. Biomolecular adducts (DNA, proteins, and lipids) formed due to reaction with ROS can be used to determine oxidative stress levels. Based on the strong correlation between oxidative stress and CKD, reversal of oxidative stress is being explored as a major therapeutic option. Xanthine oxidase inhibitors, dietary antioxidants, and other agents that scavenge free radicals are gaining interest as treatment modalities in CKD patients.