Cold stress modulates redox signalling in murine fresh bone marrow cells and promotes osteoclast transformation.

Context: Alteration of redox signalling and RANK-L expression in FBMCs of mice exposed to different intensities of cold stress (15 °C, 8 °C and 4 °C) were studied.Objective: To understand the effects of varying intensities of cold stress on murine FBMCs and its impact on osteoclastogenesis.Materials and methods: FBMCs were isolated from mice exposed to different intensities of cold stress and used for immunoblotting and biochemical assays. Bone histometry was also done.Results: Different intensities of cold stress perturb redox signalling in FBMCs and alters bone histometry. Higher RANK-L expressions were noted in FBMCs of mice exposed to 8 °C and 4 °C as compared with 15 °C.Discussion and conclusion: Cold stress boosts free radical production in FBMC's, which might enhance RANK-L expression, an indicator of osteoclastogenesis. Thus, we speculate that stronger cold stress (8 °C and 4 °C) contributes to the development of early bone loss.

Excess iodine-induced lymphocytic impairment in adult rats.

Altered lymphocytic activity and its subset ratio found responsible for initiating abnormal autoimmune responses in men and animals after excess iodine exposure. Study objective is to reveal excess iodine-induced impairment of peripheral blood lymphocytes (PBL), its functional status, antioxidant balance, DNA damage, proliferation assay, and serum cytokine levels (IL6 and TNF α)in adult male rats to understand the onset of autoimmune alterations if any indirectly that is unexplored. Experimental animals were grouped depending on doses of iodine(KI) treatment with moderately excess-7 mg/kg bw (100EI) and excessively excess-35 mg/kg bw (500EI)for 30 days to analyze IL6 and TNF α, hematological indices, oxidative stress, lymphocytic DNA damage, and proliferation status. Significant impairment in superoxide dismutase, catalase, GPx activities including elevated NO, LPO in lymphocytes of treated group, with increased IL6 and TNF α level, lymphocyte proliferation and DNA damage depending on doses of iodine. Therefore, excess iodine consumption leads to lymphocytic impairment that may be the potential cause of autoimmune thyroid diseases in long run. Highlights Excess iodine triggers the oxidative stress in lymphocytes. Excess iodine promotes the activity of pro-inflammatory cytokines. Excess iodine causes impairment of functional status of lymphocytes leading to immune-cytotoxicity. Excess iodine exacerbates the autoimmunity.

Inhibition of catalase activity with 3-amino-1,2,4-triazole intensifies bisphenol A (BPA)-induced toxicity in granulosa cells of female albino rats.

Exposure to bisphenol A (BPA), an endocrine disruptor and environmental toxicant, is associated with adverse estrogenic effects in both humans and wildlife species. Because the effects of BPA on the ovary at the cellular level are incompletely understood, the present study was designed to investigate the underlying mechanism of granulosa cell injury following BPA exposure. Eight-week-old female Wistar rats were treated with BPA (25 mg/kg BW/day for 9 days, intraperitonially) with or without pretreatment of the catalase-specific blocker 3-amino-1,2,4-triazole (ATZ; 1 g/kg BW/day for 5 days, intraperitonially). Different oxidative and antioxidant stress parameters, pro-inflammatory cytokines, and hormonal levels were measured. Catalase expression in isolated granulosa cells was analyzed by Western blot. There were noticeable increases in both nitric oxide and lipid peroxidation levels in the granulosa cells of the BPA-treated group with or without pretreatment with ATZ. Compared with the controls, BPA exposure resulted in a significant increase in pro-inflammatory cytokine levels that was further increased following pretreatment with ATZ. Results of the hormonal assays clearly showed a significant decrease in both estrogen and progesterone levels. In contrast, there was a significant increase in both serum follicle-stimulating hormone and luteinizing hormone levels following BPA exposure, with or without ATZ pretreatment. Results of Western blot analysis demonstrated decreased expression of catalase in the BPA-treated group and a further decrease in expression in the group treated with both BPA and ATZ. Our data suggest that catalase plays a role in mediating reproductive damage to granulosa cells exposed to BPA.

Iodine in excess in the alterations of carbohydrate and lipid metabolic pattern as well as histomorphometric changes in associated organs.

Background Iodine is a nonpareil constituent of thyroid hormones (THs) and a prime regulator of thyroid gland functioning. Although essential at recommended levels for the prevention of iodine deficiency disorders (IDDs), exposure to excess iodine reportedly causes hypothyroidism, hyperthyroidism, and several other emerging deleterious impacts. The objective of the present study is to explore the influence of excess iodide exposure on carbohydrate and lipid metabolism along with the histoarchitecture of certain associated organs such as the pancreas, liver, kidney, and skeletal and cardiac muscle because information on those aspects was found to be scanty. Methods Twelve rats were taken, six were fed with iodine through gavage at a dose of 3.5 mg potassium iodide (KI)/100-g body weight, which corresponded to 500 times of the physiological daily dosage of iodide for a period of 60 days, while the other six formed the control group. Results KI-treated rats presented high body weight and urinary iodine with low TH levels, suggesting a primary thyroid dysfunction. There was an increase in blood glucose, cholesterol, triglycerides, low density lipoprotein (LDL), and very low density lipoprotein (VLDL), while high density lipoprotein (HDL) levels decreased. Tissue glycogen content in the liver and skeletal muscle was decreased and was increased in the heart and kidney. Histological sections of the pancreas showed a complete disruption with hardly recognizable histoarchistructure. Treated liver sections displayed the broadened central vein with degenerated hepatocytes, while skeletal muscle sections showed dissolution of muscle fibre cells linked with loss of glycogen from these organs. Histological changes in the heart include features similar to those of a fatty heart with cardiac muscles mutilation, while that of the kidney shows an increase in glomerular tuft size and Bowman's space expansion with general deterioration. Conclusions It may thus be concluded that excess iodine exposure for a long duration causes the development of a biochemical state of hypothyroidism. The developed hypothyroidism was found responsible for the hyperglycaemic and hypercholestromic status evident by high blood glucose and cholesterol levels and the depletion of glycogen at its storage sites in the liver and skeletal muscle but the extra deposition in the cardiac muscle and kidney; histomicrophotographs showed severe destruction of the pancreatic structure. All these alterations are conducive for the pathogenesis of cardiovascular and kidney diseases.