The effects of thyroid deficiency (Td) and of chemical sympathectomy (Sx) were studied on marker enzymes of energy metabolism in cardiac muscle of neonatal and of adult rats. Td prevented the normal development of neonatal body weight, relative heart mass, and cardiac levels of cytochrome c (-22%), citrate synthase (-27%), phosphofructokinase (-20%) and Mg2+- and Ca2+-ATPase activity of purified myofibrils (-33%, -44%). Exogenous thyroxin replacement restored those parameters studied to normal with the exception that it persistently elevated citrate synthase activity significantly above normal control levels. Responses similar to those of Td neonates occurred when adult rats were similarly treated. Sx produced no consistent effects on respiratory and glycogenolytic marker enzymes, but caused a 20% reduction in Ca2+-ATPase activity of both neonatal and adult cardiac myofibrils. These findings suggest that cardiac muscle cells require thyroxin for normal growth and enzyme development. Also, Sx may impair cardiac functional capacity by altering Ca2+ activity of actomyosin ATPase.
Allopurinol is a potent xanthine oxidase inhibitor that has been administered to animals to protect tissues from oxidant injury. We hypothesized that allopurinol may protect against oxidant injury by inhibiting the inflammatory response. Male Sprague-Dawley rats were injected daily with vehicle or allopurinol and compared with noninjected controls. Animals were exposed to room air or 90% oxygen for 14 days. At the end of the exposure period, all animals were lavaged and bronchoalveolar lavage fluid (BALF) was examined for cell counts, lactate dehydrogenase (LDH), and protein. BALF neutrophils were significantly increased in oxygen-exposed noninjected controls (33 +/- 7 x 10(3)/mm3) and also in the vehicle-inoculated oxygen-exposed animals (43 +/- 6 x 10(3)/mm3). Allopurinol treatment resulted in a decrease in the neutrophilic alveolar response in oxygen-exposed animals (5.3 +/- 4 x 10(3)/mm3, P < 0.001). These data reveal that oxygen exposure produces a neutrophilic alveolar response that is attenuated by allopurinol treatment. BALF protein and LDH were significantly increased in all inoculated and noninoculated oxygen-exposed animals compared with air-exposed animals. Therefore, allopurinol decreases the neutrophilic alveolar response produced by a hyperoxic exposure in the rat but does not decrease lung injury as assessed by alveolar LDH and protein release.
Vitamin D (VD) & certain flavonoids have been shown to act directly on adipocytes & osteoblasts. In this study, we investigated whether a diet using a combination of flavonoids with VD would inhibit bone loss & decrease adiposity to a greater extent than control or VD alone diets. Ovariectomized (OVX) female rats (12 mo old, N=10, initial BW=240g) were given control (AIN‐93M diet alone), VD (10 IU/kg BW/d) or VD + resveratrol (R: 4, 20, or 100 mg/kg BW/d) + quercetin (Q: 20, 125 or 625 mg/kg BW/d) + genistein (G:16, 64 or 256 mg/kg BW/d) in AIN‐93M diet for 8 wk. After rats were killed, inguinal (I) & retroperitoneal (RP) fat pads were weighed & bones were collected for measurements. The high dose combination treatment (VD+R100+Q625+G256) significantly reduced BW gain (79±5 vs 62±3g, p<0.05), weight of RP+I fat pads (21.8±1 vs 19.8±0.8g, p<0.05) & RP+I fat pads as % of BW (7.5±0.4 vs 6.9±0.4%, p<0.05). Bone mineral density (BMD) & content (BMC) of femora were significantly increased by the high dose combination, although they weren't different from VD alone. However, BMD corrected for BW was significantly greater in the high dose treated group compared to both control & VD groups (4.7±0.05 vs 5.0±0.2 vs 5.6±0.2, p<0.05). We conclude that VD when combined with R, Q & G improved bone density & reduced weight gain & adiposity in OVX female rats compared to control & VD alone. Supported by the GA Research Alliance Eminent Scholar endowment (CAB).
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